Splenectomy in an uraemic patient with acquired factor X deficiency due to AL amyloidosis.
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Amyloidosis↗
Biomedical subjects
J Lin
Publications and source records attributed to J Lin.
Treatment of humeral shaft fractures with humeral locked nail and comparison with plate fixation.
OBJECTIVE: To report the experience of a newly devised humeral locked nail in treating acute humeral shaft fractures and to compare its effectiveness with that of plate fixation. DESIGN AND METHODS: Data were collected on 48 acute humeral shaft fractures in 48 consecutive patients treated with humeral locked nails and compared with retrospective data on 25 fractures in 25 other patients treated with dynamic compression plates. The operation time, amount of blood transfusion, time to union, complications, and functional recovery were recorded and compared. The average follow-up time was 20.5 months for the nail group and 33.3 months for the plate group. Student's t test and Fisher's Exact Test were used for statistical analyses. RESULTS: Locked nailing had significantly shorter operation time and less blood transfusion than did plate fixation, 68 versus 93 minutes and 0 versus 102 mL, respectively. Eventual union was achieved among all in the nail group and among all but one in the plate group. Union rate and time to union were not significantly different. In the plate group, three fractures had complications: one with implant loosening and nonunion, one with deep infection, and one with postoperative radial nerve palsy; the nail group had no complications. The difference in complication rates was statistically significant. In the nail group, one varus malunion and one intraoperative comminution occurred, without adverse consequences. Functional recovery was essentially the same in both groups for uncomplicated fractures. CONCLUSIONS: Humeral locked nailing offered a less invasive surgical technique and more favorable treatment results than did plate fixation. Correct nailing direction, precise surgical techniques, less bulky hardware, and stable transfixing screws are the keys to a successful treatment. Further prospective, randomized comparative study is warranted.
Adult↗
Locked nailing for displaced surgical neck fractures of the humerus.
OBJECTIVE: To report experience with a newly devised humeral locked nail for treating surgical neck fractures of the humerus. This device has the advantages of a small diameter for minimal tissue trauma and transfixing locking screws for reliable fixation. METHODS: From 1993 to 1996, 21 consecutive severely displaced surgical neck fractures of the humerus were antegrade nailed with humeral locked nails; 2 fractures were associated with dislocation and 1 fracture was a comminuted metaphyseal fracture with a failed plating. The average age of patients was 65.8 years; average follow-up time was 19.2 months. The proximal screws were applied upward in 5 patients and downward in 16 patients. Static locking was performed in 8 patients, dynamic locking in 13 others. RESULTS: The average operation time was 55 minutes. No patients needed blood transfusion. All fractures eventually achieved union with an average time to union of 14.8 weeks. On the basis of Neer criteria for outcome analysis, excellent or satisfactory results were obtained for 86% of the patients (18 of 21 patients). No patients had deep infection, implant failure, malunion, osteonecrosis, or nail migration that interfered with joint motion. Due to technique errors, one patient had shoulder joint impingement caused by protrusion of the proximal nail tip. CONCLUSION: The operative method reported here has the advantages of minimal tissue trauma, minimal hardware application, sufficient fixation, and easy operative technique, and it can be a worthy alternative for the treatment of severely displaced surgical neck fractures of the humerus.
Adult↗
Expression of glycoconjugates in human eustachian tubes with otitis media.
OBJECTIVES: To characterize glycoconjugate expression in normal human eustachian tubes and study the alterations in glycoconjugate expression found in eustachian tubes with otitis media. STUDY DESIGN: Using lectin histochemistry, alterations in glycoconjugates were studied in three normal temporal bones, in four temporal bones with mucoid otitis media (MOM), and in five with serous otitis media (SOM). METHODS: Sections of previously processed temporal bones were decelloidinized, and then incubated with seven biotinylated lectins--WGA, SNA, MAA, BPA, PNA, UEA-1, and LcH--that reflect seven carbohydrate residues of glycoconjugates, respectively: GlcNAc/NeuNAc, NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, Gal beta(1-3) GalNAc, L-fucose, and alpha-mannose residues. Control sections were incubated with inhibitory carbohydrates or without biotinylated lectins. RESULTS: In the normal temporal bones, five carbohydrate residues in goblet cells and cilia of the eustachian tube demonstrated moderate to strong activity--NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, GalNAc, Gal beta(1-3)GalNAc, and L-fucose. Two residues demonstrated weak activity--GlcNAc/NeuNAc and alpha-mannose. Temporal bones with MOM revealed increases in sialic acid and alpha-mannose, and a decrease in L-fucose. Residues of carbohydrates in the cilia of bones with SOM were notably decreased, especially for GalNAc, Gal beta(1-3)GalNAc, and NeuNAc alpha(2-6)GalNAc. CONCLUSIONS: Glycoconjugates in the normal human eustachian tube are rich in GalNAc, Gal beta(1-3)GalNAc, L-fucose, and NeuNAc alpha(2-3/2-6) GalNAc, but low in alpha-mannose and sialic acid. Eustachian tubes from cases with SOM or MOM demonstrated alterations in glycoconjugate expression in cilia and goblet cells, which may reflect disorder of the carbohydrate metabolism during otitis media, especially in SOM.
Eustachian Tube↗
Variants of N-acetyltransferase NAT1 and a case-control study of colorectal adenomas.
N-acetyltransferase NAT1, together with enzymes CYP1A2 and NAT2, helps convert heterocyclic amines to mutagens. Epidemiologic studies of the association of variants of these enzymes with colorectal cancer may provide indirect support for a heterocyclic amine mechanism. We used single strand conformation polymorphism and heteroduplex analysis to screen fro mutations in the NAT1 coding region in a case-control study (n = 932) of colorectal adenomas, which are precursors to cancer. Thirteen different single-base mutations were found: C97T, C190T, T402C, G445A-G459A-T640G ( a combination of three mutations), C559T, G560A, A613G, A752T, T777C, G781A, and A787G. Function of novel mutations was tested by bacterial production of enzymes and measurements of Km, Vmax, and stability. However, on 24-control individuals and 18 cases carried an inactivating NAT1 mutation. When combined with our data on the NAT2 acetylation polymorphism, we saw no evidence for an association between N-acetyltransferases and prevalence of adenomas. Larger sample sizes are required for further evaluation.
Acetyltransferases↗
Morphometric texture analysis of spinal trabecular bone structure assessed using orthogonal radiographic projections.
The measurement of bone microstructure as well as bone mineral density may improve the estimation of bone strength. Cubic specimens (N = 26, 12 mm X 12 mm X 12 mm) of human cadaver vertebrae were cut along three orthogonal anatomic orientations, i.e., superior-inferior (SI), medial-lateral (ML), and anterior-posterior (AP). Contact radiographs of the bone cubes along all three orientations were obtained and then digitized by a laser scanner with pixel size of 50 microns x 50 microns. The specimens were tested in compression along the 3 orthogonal orientations and the Young's modulus (YM) was calculated for each direction. Quantitative computed tomography (QCT) was used to obtain a measure of trabecular bone mineral density (BMD). Global gray level thresholding and local thresholding algorithms were used to extract the trabecular bone network. Apparent trabecular bone fraction (ABV/TV), mean intercept length (I.TH), mean intercept separation (I.SP), and number of nodes (N.ND) were measured from the extracted trabecular network. Fractal dimension (Fr.D) of the trabecular bone texture was also measured. Paired t-tests showed that the mean values of each texture parameter (except ABV/TV) and of YM along the SI direction were significantly different (p < 0.05) from those along the ML and AP direction. However, the mean values along the ML and AP directions were not significantly different. Multivariate regression of YM as a function of the texture parameters and BMD showed that without adjusting for the effect of BMD, YM was significantly explained by all the texture parameters (R2 = 0.2-0.6). When BMD was included in the regression, although the variations in YM of ML, AP, and SI orientations could be explained by BMD alone, some of the texture parameters did improve the overall prediction of the biomechanical properties, while, some parameters such as ABV/TV and Fr.D in the ML orientation showed a more significant overall effect in explaining mechanical strength than did BMD. In conclusion, trabecular texture parameters correlated significantly with BMD and YM. Trabecular texture parameters from projectional radiographs reflect the anisotropy of trabecular structure. Quantitative radiographic assessment of trabecular structure using fine-detail radiography can potentially improve the estimation of bone strength.
Adult↗
I-PpoI, the endonuclease encoded by the group I intron PpLSU3, is expressed from an RNA polymerase I transcript.
PpLSU3, a mobile group I intron in the rRNA genes of Physarum polycephalum, also can home into yeast chromosomal ribosomal DNA (rDNA) (D. E. Muscarella and V. M. Vogt, Mol. Cell. Biol. 13:1023-1033, 1993). By integrating PpLSU3 into the rDNA copies of a yeast strain temperature sensitive for RNA polymerase I, we have shown that the I-PpoI homing endonuclease encoded by PpLSU3 is expressed from an RNA polymerase I transcript. We have also developed a method to integrate mutant forms of PpLSU3 as well as the Tetrahymena intron TtLSU1 into rDNA, by expressing I-PpoI in trans. Analysis of I-PpoI expression levels in these mutants, along with subcellular fractionation of intron RNA, strongly suggests that the full-length excised intron RNA, but not RNAs that are further cleaved, serves as or gives rise to the mRNA.
Animals↗
Identification of a novel slow-muscle-fiber enhancer binding protein, MusTRD1.
The molecular mechanisms which are responsible for restricting skeletal muscle gene expression to specific fiber types, either slow or fast twitch, are unknown. As a first step toward defining the components which direct slow-fiber-specific gene expression, we identified the sequence elements of the human troponin I slow upstream enhancer (USE) that bind muscle nuclear proteins. These include an E-box, a MEF2 element, and two other elements, USE B1 and USE C1. In vivo analysis of a mutation that disrupts USE B1 binding activity suggested that the USE B1 element is essential for high-level expression in slow-twitch muscles. This mutation does not, however, abolish slow-fiber specificity. A similar analysis indicated that the USE C1 element may play only a minor role. We report the cloning of a novel human USE B1 binding protein, MusTRD1 (muscle TFII-I repeat domain-containing protein 1), which is expressed predominantly in skeletal muscle. Significantly, MusTRD1 contains two repeat domains which show remarkable homology to the six repeat domains of the recently cloned transcription factor TFII-I. Furthermore, both TFII-I and MusTRD1 bind to similar but distinct sequences, which happen to conform with the initiator (Inr) consensus sequence. Given the roles of MEF2 and basic helix-loop-helix (bHLH) proteins in muscle gene expression, the similarity of TFII-I and MusTRD1 is intriguing, as TFII-I is believed to coordinate the interaction of MADS-box proteins, bHLH proteins, and the general transcription machinery.
Amino Acid Sequence↗
Quantitation and regulation of pyroglutamyl peptidase II messenger RNA levels in rat tissues and GH3 cells.
The distribution of the mRNA of the specific thyrotropin-releasing-hormone (TRH)-degrading enzyme pyroglutamyl peptidase II (EC 3.4.19.6) in rat tissues and brain regions and its regulation in rat tissues and in GH3 cells was studied by a reliable and quantitative solution hybridization ribonuclease protection assay. The distribution of pyroglutamyl peptidase II mRNA levels was uneven with the highest level of mRNA found in brain. Within brain the distribution of pyroglutamyl peptidase II mRNA was heterogeneous. A single dose of T3 markedly increased the level of pyroglutamyl peptidase II mRNA in the pituitary (p < 0.01) and in the liver (p < 0.05). In GH3 cells, exposure to T3 at concentrations from 10(-10) to 10(-6) M for time periods of 2-24 h, did not change pyroglutamyl peptidase II mRNA levels. Acute administration of TRH to rats had no effect on pyroglutamyl peptidase II mRNA levels. By contrast, TRH down-regulated pyroglutamyl peptidase II mRNA in GH3 cells. A similar effect was produced in GH3 cells by activators of protein kinase C. These studies reveal fundamental differences in the mechanism of regulation of pyroglutamyl peptidase II mRNA in pituitary and in GH3 cells. Elevation of pyroglutamyl peptidase II mRNA in liver by T3 suggests that this organ is the source of the enzyme in serum.
Aminopeptidases↗
Increase of mucous glycoprotein secretion by tumor necrosis factor alpha via a protein kinase C-dependent mechanism in cultured chinchilla middle ear epithelial cells.
Tumor necrosis factor alpha (TNF-alpha), originally defined by its antitumoral activity, is now recognized as a polypeptide mediator of inflammatory and cellular immune response. Recent studies have demonstrated that TNF-(alpha exists in the fluid of otitis media with effusion and, therefore, suggested its possible role in the pathogenesis of mucus hypersecretion. In this study, the effects of TNF-alpha on mucous glycoprotein (MGP) secretion from cultured chinchilla middle ear epithelial cells were examined, and TNF-alpha was found to stimulate MGP secretion in a time- and concentration-dependent manner. The action of TNF-alpha on MGP secretion was significantly and dose-dependently inhibited by TNF-alpha monoclonal antibody; this finding is suggestive of its specificity on MGP secretion. The addition of the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperidine (H-7) to the culture significantly blocked TNF-alpha-induced MGP secretion, while the calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) did not. This suggests that TNF-alpha stimulates MGP secretion via a protein kinase C-dependent mechanism.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Identification of trophoblast-specific regulatory elements in the mouse placental lactogen II gene.
Placental lactogen II, the major ligand for the PRL receptor during the second half of gestation in rodents, is synthesized specifically by placental trophoblast giant cells. A transient transgenic analysis has been used to localize the giant cell-specific regulatory region within the mouse placental lactogen II gene to sequences between -1340 and -2019 upstream of the transcriptional start site. More precise mapping of the regulatory elements has been accomplished by transfection of promoter constructs into Rcho-1 trophoblast cells, resulting in the characterization of two positive regulatory elements in the -1471 to -1340 region; two other regulatory elements have been implicated but not further characterized, a negative regulatory element between -2019 and -1778 and another positive element within the region from -1340 to -569. Both of the characterized positive regulatory elements are recognized by factors that are enriched in differentiated giant cells compared with proliferative trophoblasts, and these factors are either absent or at low levels in fibroblasts. The complexes that form on the two elements are distinct and neither element competes with the other for factor binding, thus implicating at least two different regulatory elements in late-gestational trophoblast giant cell-specific gene expression.
Animals↗
Electromyographic investigation of masticatory muscles in unilateral cleft lip and palate patients with anterior crossbite.
OBJECTIVE: To evaluate the characteristics of masticatory muscle activity in operated unilateral cleft lip and palate (UCLP) patients with anterior crossbite compared with normal individuals. SUBJECTS: Sixteen male and 13 female Chinese patients with UCLP and anterior crossbite. Fifteen male and 13 female Chinese individuals without cleft abnormalities served as a control group. DESIGN: Electromyographic activity of the masseter muscles and anterior temporalis muscles was recorded bilaterally in different mandibular positions using bipolar surface electrodes. RESULTS: Compared to noncleft controls, patients with UCLP demonstrated (1) higher activation levels of masseter and temporalis muscles in the rest position, (2) lower potential function of masseter and temporalis, (3) inharmonious activity of the masticatory muscles during mandibular border movement, (4) a higher asymmetry index of the masseter and temporalis muscles, and (5) longer silent periods of the two muscles. CONCLUSIONS: The function of masticatory muscles is different in patients with UCLP with anterior crossbite. Muscle function should be considered when evaluating cleft patients for orthodontic treatment and orthognathic surgery.
Action Potentials↗
Osteochondromalike parosteal osteosarcoma: a report of six cases of a new entity.
OBJECTIVE: Our purpose was to describe a rare juxtacortical bone sarcoma with deceptively benign, osteochondromalike histologic characteristics. We present criteria by which this low-grade malignant neoplasm can be distinguished from other benign and malignant surface lesions of bone with particular emphasis on the imaging features. MATERIALS AND METHODS: Six cases of a low-grade, chondroossifying parosteal sarcoma of bone were reviewed. Patients included four males and two females 11 months to 66 years old. Histologic findings from initial tumors and from recurrent tumors were reviewed. Two musculoskeletal radiologists analyzed the imaging studies, which included plain films, CT scans, MR images, and a bone scan. RESULTS: Histologically, the lesions were characterized by a thin layer of proliferating, periosteally derived spindle cells overlying a thin, low-grade malignant cartilage cap that underwent calcification, neovascularization, and conversion into benign bone and marrow fat. These lesions were unique in that the malignant elements were only at their periphery. All six cases were initially misdiagnosed as benign lesions on pathologic evaluation. In each patient, imaging revealed a "pasted-on" ossified surface lesion with an intact underlying cortex and no medullary involvement. In three cases, recurrent tumors had histologic appearances consistent with conventional parosteal osteosarcoma. Dedifferentiation, metastases, and death occurred in one of these three cases. CONCLUSION: To our knowledge, this surface lesion of bone has not been specifically described. Whether this tumor constitutes a distinct entity or is a specialized variant of parosteal osteosarcoma is unclear. Precise radiologic-pathologic correlation is essential for appropriate diagnosis and management.
Adolescent↗
Upregulation of the vascular endothelial growth factor/vascular endothelial growth factor receptor system in experimental background diabetic retinopathy of the rat.
Vascular endothelial growth factor (VEGF) is a major contributor to retinal neovascularization. The possible participation of VEGF and its high-affinity tyrosine kinase receptors, flk-1 and flt-1, in early background diabetic retinopathy was studied in the streptozotocin-induced diabetic rat model of experimental retinopathy using in situ hybridization, blotting techniques, and immunohistochemistry. Diabetic retinopathy was assessed by quantitative morphometry of retinal digest preparations. The number of acellular capillaries increased 2.7-fold in diabetic animals with diabetes' duration of 6 months compared with nondiabetic controls. VEGF expression was not detectable by in situ hybridization in nondiabetic rats but was highly increased in the ganglion cell layer and in the inner and outer nuclear layers of retinas from diabetic animals. VEGF protein was extractable only from diabetic retinas, and a strong immunolabeling was detected in vascular and perivascular structures. Increased flk-1 and flt-1 mRNA levels were also found in the ganglion cell and both nuclear layers of diabetic samples only. Dot blot and Western blot analyses confirmed the increase in flk-1 mRNA and protein in diabetic retinas. Also, flk-1 immunoreactivity was associated with vascular and nonvascular structures of the inner retinas from diabetic animals. These data obtained from a rodent model in which retinal neovascularization does not occur support the concept that the VEGF/VEGF receptor system is upregulated in early diabetic retinopathy.
Animals↗
Inhibition of in vitro growth of coliform bacteria by a monoclonal antibody directed against ferric enterobactin receptor FepA.
The ability of a murine monoclonal antibody that blocks the enterobactin ligand-binding site of the ferric enterobactin receptor FepA to inhibit the growth of coliform bacteria derived from a bovine intramammary infection (IMI) was determined in an iron-restricted medium. Bacterial isolates from bovine IMI in five herds were tested by the chrome azurol sulfonate assay to detect siderophore production. Each of the isolates of Escherichia coli (n = 25) and Klebsiella pneumoniae (n = 25) were positive for siderophore production. Each isolate expressed iron-regulated outer membrane proteins when grown in trypticase soy broth plus the iron chelator alpha-alpha'-dipyridyl. Immunoblots revealed that the monoclonal antibody recognized FepA that was expressed by each of the E. coli isolates (n = 25). Only 4 of 25 K. pneumoniae isolates produced FepA that reacted with the monoclonal antibody. This result coincided with the results of an in vitro growth assay. Growth of all E. coli isolates was significantly inhibited by the addition of monoclonal antibody to synthetic medium containing apolactoferrin. Antigenic variation in the enterobactin-binding site resulted in a low percentage of K. pneumoniae isolates that were inhibited by the monoclonal antibody. Inhibition of bacterial growth by the monoclonal antibody was dose-dependent. As little as 50 micrograms/ml of purified antibody had an inhibitory effect on bacterial growth in the synthetic iron-restricted medium. Monoclonal antibody specific for the enterobactin ligand-binding site of FepA inhibited the growth of E. coli that was isolated from bovine IMI.
Animals↗
Immunization of cows with ferric enterobactin receptor from coliform bacteria.
The serum and milk immunoglobulin (Ig) G responses of lactating dairy cows were determined following immunization with ferric enterobactin receptor FepA. Escherichia coli 471 was cultured in iron-depleted medium, and outer membrane proteins were extracted by 2% N-lauroylsarcosine sodium salt and 2% Triton X-100. The FepA was isolated from the outer membrane proteins by ion-exchange chromatography. Twenty cows were assigned to four treatment groups of 5 cows blocked by breed and days in milk. Treatment groups were vaccinated with 100 micrograms of FepA, 500 micrograms of FepA, Escherichia coli J5 bacterin, or sterile phosphate-buffered saline. Primary immunization was at approximately 200 d in milk, and booster immunizations were given 14 and 28 d later. Serum and whey IgG titers to FepA in cows vaccinated with FepA were significantly higher than those from cows vaccinated with either E. coli J5 bacterin or phosphate-buffered saline. Serum and whey IgG titers to FepA were elevated by 14 d in cows vaccinated with FepA. Significant differences were not observed between doses of FepA. The degree of cross-reactivity of purified IgG from cows vaccinated with FepA to E. coli and Klebsiella pneumoniae isolates was significantly higher than that to a control isolate that lacked FepA production. Immunization with FepA elicited an immunological response in serum and milk.
Ammonium Sulfate↗
[Experimental study of effects of anti-ovarian antibodies on ovarian histology and function].
OBJECTIVE: To investigate the effects of anti-ovarian antibodies (AOA) on ovarian histology and functions. METHODS: Rabbit antibodies against mice ovarian tissues were obtained by immunizing with mice ovarian extracts and purified. The effects of AOA on mice ovarian histology were examined under light and electronic microscope. In addition, changes of ovarian functions, including natural pregnant rate and pregnant mare serum gonadotropin (PMSG) + hCG induced ovulation rate and pregnant rate, were also observed. RESULTS: After treating with different doses of AOA pathological changes occurred in a variety of ovarian components, especially in zona pellucida and granulosa cells, which is more serious in high AOA level group than that in low AOA level group. The natural pregnant rate decreased to zero in both AOA groups. The ovulation and pregnant rate induced by PMSG-hCG were significant lower in both AOA groups than that in the control group especially in the high AOA level group. CONCLUSION: AOA may damage the ovarian tissues and reduce the ovulation and pregnant rate. The higher the AOA level, the more serious pathological changes and the poorer curative effects of PMSG-hCG may occur.
Animals↗
[Determination of cellular and humoral immunity in mice of autoimmune ovarian failure].
OBJECTIVE: To determine cellular and humoral immunity in mice of autoimmune ovarian failure. METHODS: A mice model of autoimmune ovarian failure was established. The percentages of help T cell (CD4+) and suppressor T cell (CD8+), the ratio of CD4/CD8 and anti-ovarian antibody (AOA) were determined. RESULTS: No significant changes were found in CD4+ fraction, but the percentage of CD8+ was reduced and the ratio of CD4/CD8 increased. AOA was positive which was probably the cause of damage of the ovarian tissues, reduction of sex hormone secretion and impaired fertility. CONCLUSION: Autoimmune ovarian failure is correlated with the abnormal change of CD4/CD8 and the increase of B-lymphocytes function.
Animals↗