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Biomedical subjects

Q Chen

Publications and source records attributed to Q Chen.

At least 595 records · Page 33Linked to original sources
PubMed1995

Anterior decompressive surgery for cervical ossified posterior longitudinal ligament causing myeloradiculopathy.

This paper reviews 88 patients (74 males and 14 females) who underwent anterior decompression and fusion for symptomatic ossified posterior longitudinal ligament of the cervical spine. Follow up averaged 8.5 years. Eighteen patients underwent one-vertebra, 59 two-vertebra, and 11 three-vertebra decompression with interbody fusion. The preoperative severity of symptoms significantly affected neurological recovery. Patients with three-vertebra spondylectomy showed significantly little neurological improvement. The return of patients to their previous activities as monitored at follow up was related to their preoperative neurological status. MRI findings appeared to be relevant to neurological recovery. Our findings suggest that anterior decompression is to be recommended for patients with less advanced preoperative symptoms and the involvement of one or two vertebrae.

Activities of Daily Living↗
PubMed1995

Cervical laminoplasty in patients with ossification of the posterior longitudinal ligaments.

Cervical laminoplasty was the operation used for myeloradiculopathy secondary to ossification of the posterior longitudinal ligaments. Some 57 patients were followed up for 5-13 years (average: 7.8 years). The spinal canal from C3 to C7 was surgically opened en bloc unilaterally with spacer bone grafting to maintain the laminae in a 'kept open' position and thus to implement posterior decompression. No serious major surgery-related complications were observed. Favourable results were obtained in 42 patients (74%), but those with advanced preoperative neurological symptoms did not improve. Patients with spinal canals seriously compromised by anterior ossified lesions recovered poorly. We concluded that laminoplasty is recommended for cervical myeloradiculopathy due to ossified posterior longitudinal ligaments for selected patients, but surgery should be done before the patient has developed serious neurological damage.

Aged↗
PubMed1995

Cartilage matrix protein forms a type II collagen-independent filamentous network: analysis in primary cell cultures with a retrovirus expression system.

Cartilage matrix protein (CMP) is expressed specifically in mature cartilage and consists of two von Willebrand factor A domains (CMP-A1 and CMP-A2) that are separated by an epidermal growth factor-like domain, and a coiled-coil tail domain at the carboxyl terminal end. We have shown previously that CMP interacts with type II collagen-containing fibrils in cartilage. In this study, we describe a type II collagen-independent CMP filament and we analyze the structural requirement for the formation of this type of filament. Recombinant wild-type CMP and two mutant forms were expressed in chick primary cell cultures using a retrovirus expression system. In chondrocytes, the wild-type virally encoded CMP is able to form disulfide bonded trimers and to assemble into filaments. Filaments also form with CMP whose Cys455 and Cys457 in the tail domain were mutagenized to prevent interchain disulfide bond formation. Therefore, intermolecular disulfide bonds are not necessary for the assembly of CMP into filaments. Both the wild-type and the double cysteine mutant also form filaments in fibroblasts, indicating that chondrocyte-specific factors are not required for filament formation. A truncated form of CMP that consists only of the CMP-A2 domain and the tail domain can form trimers but fails to form filaments, indicating that the deleted CMP-A1 domain and/or the epidermal growth factor domain are necessary for filament assembly but not for trimer formation. Furthermore, the expression of the virally encoded truncated CMP in chondrocyte culture disrupts endogenous CMP filament formation. Together these data suggest a role for CMP in cartilage matrix assembly by forming filamentous networks that require participation and coordination of individual domains of CMP.

Amino Acid Sequence↗
PubMed1995

Brain iron, transferrin and ferritin concentrations are altered in developing iron-deficient rats.

To study the iron, transferrin, and ferritin distribution at subcellular levels in response to acute dietary iron deficiency, we tested the hypothesis that early post-weaning iron deficiency can change iron and iron regulatory protein concentrations in rat brain. Male Sprague-Dawley rats were fed diets containing either 2 or 35 micrograms iron/g for 2, 3 or 4 wk starting at 21 d of age. Brain iron, transferrin and ferritin concentrations in cytosolic and microsomal fractions of either whole brain or pons and cerebellum were then determined. After 14 d of dietary iron restriction, brain iron concentrations were 50% lower in the microsomal fraction and 30% lower in cytosol compared with controls. Brain cytosolic transferrin concentration almost doubled in the same animals. Brain ferritin concentration in fractions from rats fed the iron-deficient diet for 14 d was lower than in controls, but then remained fairly constant. Absolute brain weight and total brain protein contents were unaffected by iron restriction. This study extends previous research by demonstrating that the brain responds to changes in body iron status with a change in transferrin concentration. If the dietary restriction is quite severe, this adaptation is insufficient. This study also notes that brain ferritin decreases with decreasing body iron status, though it was less responsive than nonheme iron in liver. The concept that iron enters the brain through a highly regulated endocytotic process at the blood brain barrier, that undoubtedly involves the regulation of transferrin receptors in capillary endothelial cell, is supported by our observation of elevated transferrin concentrations in brain of iron-deficient rats.

Anemia, Iron-Deficiency↗
PubMed1995

Antisense RNA regulation of the fatB iron transport protein gene in Vibrio anguillarum.

We have recently identified an antisense RNA (RNA alpha) that regulates the expression of the fatA iron transport gene encoding the outer membrane receptor for the iron-anguibactin complex. In this work, we demonstrate that RNA alpha also inhibits the expression of fatB, which encodes a 35 kDa iron transport protein and has domains homologous to other periplasmic transport proteins. The expression of fatA and fatB is repressed under iron-rich conditions, in which RNA alpha is induced. RNA alpha is homologous to two-thirds of the coding region of fatB. By cloning RNA alpha coding sequences immediately downstream of a tet promoter, we were able to obtain constitutive expression of the antisense RNA. The cloned region contains approximately 83% of the 650 nucleotide RNA alpha and is complementary to only 51% of the fatB mRNA but is still capable of causing a repression of the expression of the fatB gene. Our results in this work demonstrate that RNA alpha probably affects the stability of the fatB-specific mRNA.

Bacterial Proteins↗
PubMed1995

Growth on octane alters the membrane lipid fatty acids of Pseudomonas oleovorans due to the induction of alkB and synthesis of octanol.

Growth of Pseudomonas oleovorans GPo1, which contains the OCT plasmid, on octane results in changes in the membrane phospholipid fatty acid composition. These changes were not found for GPo12, an OCT-plasmid-cured variant of GPo1, during growth in the presence or absence of octane, implying the involvement of OCT-plasmid-encoded functions. When recombinant strain GPo12(pGEc47) carrying the alk genes from the OCT plasmid was grown on octane, the cells showed the same changes in fatty acid composition as those found for GPo1, indicating that such changes result from induction and expression of the alk genes. This finding was corroborated by inducing GPo12(pGEc47) with dicyclopropylketone (DCPK), a gratuitous inducer of the alk genes. Further experiments showed that the increase of the mean acyl chain length of fatty acids is related to the expression of alkB, which encodes a major integral membrane protein, while the formation of trans unsaturated fatty acids mainly results from the effects of 1-octanol, an octane oxidation product.

1-Octanol↗
PubMed1995

An AU-rich element in the 3' untranslated region of the spinach chloroplast petD gene participates in sequence-specific RNA-protein complex formation.

In chloroplasts, the 3' untranslated regions of most mRNAs contain a stem-loop-forming inverted repeat (IR) sequence that is required for mRNA stability and correct 3'-end formation. The IR regions of several mRNAs are also known to bind chloroplast proteins, as judged from in vitro gel mobility shift and UV cross-linking assays, and these RNA-protein interactions may be involved in the regulation of chloroplast mRNA processing and/or stability. Here we describe in detail the RNA and protein components that are involved in 3' IR-containing RNA (3' IR-RNA)-protein complex formation for the spinach chloroplast petD gene, which encodes subunit IV of the cytochrome b6/f complex. We show that the complex contains 55-, 41-, and 29-kDa RNA-binding proteins (ribonucleoproteins [RNPs]). These proteins together protect a 90-nucleotide segment of RNA from RNase T1 digestion; this RNA contains the IR and downstream flanking sequences. Competition experiments using 3' IR-RNAs from the psbA or rbcL gene demonstrate that the RNPs have a strong specificity for the petD sequence. Site-directed mutagenesis was carried out to define the RNA sequence elements required for complex formation. These studies identified an 8-nucleotide AU-rich sequence downstream of the IR; mutations within this sequence had moderate to severe effects on RNA-protein complex formation. Although other similar sequences are present in the petD 3' untranslated region, only a single copy, which we have termed box II, appears to be essential for in vitro protein binding. In addition, the IR itself is necessary for optimal complex formation. These two sequence elements together with an RNP complex may direct correct 3'-end processing and/or influence the stability of petD mRNA in chloroplasts.

Base Sequence↗
PubMed1995

Direct G protein activation reverses impaired CCK signaling in human gallbladders with cholesterol stones.

Human gallbladders were used to investigate the mechanisms of the impaired contraction induced by cholecystokinin (CCK) associated with cholesterol stones. Single muscle cells were isolated enzymatically with collagenase. Inositol 1,4,5-trisphosphate was measured by high-performance liquid chromatography. Diacylglycerol was assayed by thin-layer chromatography. CCK stimulation showed decreased muscle contraction and production of inositol 1,4,5-trisphosphate and diacylglycerol in gallbladders with cholesterol stones compared with those with pigment stones. Exogenous calmodulin induced maximal contraction of 22.4 +/- 0.5 and 21.0 +/- 0.6% in gallbladders with cholesterol and pigment stones, respectively. Similar findings were observed with a synthetic diacylglycerol analogue. Two G protein activators, aluminum fluoride and guanosine 5'-O-(3-thiotriphosphate), evoked similar responses in these two types of gallbladders, with maximal contractions of 21.3 +/- 0.4 and 23.3 +/- 0.5%, respectively, in those with cholesterol stones and 20.9 +/- 0.8 and 22.6 +/- 0.4%, respectively, in those with pigment stones. These results suggest that receptor-dependent ligands like CCK cannot fully activate the intracellular pathways, which, however, can be fully stimulated by circumventing receptors with G protein activators or second messengers. After G protein activation, the pathways appear to be functionally intact. The defect might then reside in the receptor or in the interaction between receptors and G proteins.

Aluminum Compounds↗
PubMed1995

Regional expression of natriuretic peptide receptors during the formation of arterial neointima in the rabbit.

In vitro evidence suggests that natriuretic peptide receptors (NPR)-B and NPR-C inhibit vascular smooth muscle (VSM) proliferation. NPR-B is guanylate cyclase-coupled and selectively activated by C-type natriuretic peptide (CNP)-(1-22). NPR-C is not guanylate cyclase-coupled and, unlike NPR-B, avidly binds atrial natriuretic peptide (ANP)-(1-28) as well as CNP-(1-22). Here, we investigate these receptors during the VSM proliferation and neointimal formation found 5, 7, and 20 days after compressing the central ear artery of the rabbit. Receptors were mapped autoradiographically using [125I-Tyr0]CNP-(1-22), which binds NPR-B and NPR-C, and 125I-ANP-(1-28), which binds NPR-C and NPR-A, another guanylate cyclase-coupled receptor. Normal tunica media had NPR-B-like binding sites, and the level of these did not change significantly after compression. Consistent with this, CNP-(1-22) stimulated cGMP production equally with membranes from normal or damaged arteries and was more effective than ANP-(1-28). Neointima, which became evident 5 to 7 days after arterial damage, expressed NPR-C-like sites and no detectable NPR-B-like binding. NPR-C-like sites also appeared on the media for the first time between 5 and 7 days after compression. Immunohistochemistry for proliferating cell nuclear antigen revealed widespread mitosis in VSM at 5 days after compression, but mitosis was virtually restricted to the neointima at and beyond 7 days after compression. Thus, whereas levels of NPR-B did not change significantly after arterial injury and NPR-A was not detected, NPR-C-like receptors were upregulated as mitosis declined in the media and as a prominent neointima formed.

Animals↗
PubMed1995

Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

BACKGROUND AND PURPOSE: Serum lipoprotein(a) [Lp(a)] levels are genetically determined and considered to be an independent risk factor for atherosclerosis. The aim of this study was to provide a complete analysis of Lp(a) serum levels, apolipoprotein(a) phenotypes, and other lipid parameters for different forms of severity of symptomatic ischemic cerebrovascular disorders as well as for different stages of carotid atherosclerosis. METHODS: Lp(a) concentration, apolipoprotein(a) phenotype, triglyceride, low-density lipoprotein, high-density lipoprotein, and total cholesterol levels of blind-coded specimens as well as degree of carotid artery stenosis were assessed in a consecutive series of patients with ischemic cerebrovascular disease. We evaluated 265 male (34%) and female (66%) patients (mean age, 51 +/- 7.4 years) with transient ischemic attack (55.8%), prolonged reversible ischemic neurological deficits (28.3%), and cerebral infarction (15.9%) as well as 288 male (30%) and female (70%) control subjects (mean age, 51 +/- 7.1 years). All subjects were white. RESULTS: Lp(a), total, and low-density lipoprotein cholesterol were statistically significantly elevated in all patients compared with control subjects. Lp(a) correlated with the severity of symptomatic cerebrovascular disease and the degree of carotid stenosis. Logistic regression analysis revealed Lp(a) as the best single marker for the presence of cerebrovascular disease (P < .001) followed by high-density lipoprotein cholesterol (P = .003) and triglycerides (P = .049). With a cutoff of 20 mg/dL of Lp(a), the odds ratio for a subject to have had ischemic stroke with elevated Lp(a) was 20.3 and 23.7 depending on the method of the Lp(a) estimation, whereas the odds ratio when the sonography score was > 0 was 15.4. The investigation of the distribution of the apo(a) phenotypes revealed that 16.73% of the control subjects had major isoforms < or = 580 kD molecular weight (B, F, S1, S2) versus 42.65% of the patients' group (P < .001). These isoforms were also present in 14.71% of all individuals with a sonography score of 0 but in 52.30% of all individuals with a sonography score > 0 (P < .001). CONCLUSIONS: This case-control study shows that an elevated Lp(a) level is the primary factor associated with the presence of ischemic cerebrovascular disease and that the increased portion of the smaller-molecular-weight apo(a) isoforms in patients and individuals with a sonography score > 0 points toward an inherited predisposition for this disease.

Adult↗
PubMed1995

Interaction of metals during their uptake and accumulation in rabbit renal cortical slices.

The uptake and accumulation of metals occurs in the kidney, which is a key site for interaction between metal nephrotoxicants. The uptake/accumulation and interaction of CdCl2, HgCl2, K2Cr2O7, and NaAsO2 was examined in precision-cut rabbit renal cortical slices. Slices were incubated with 10(-6) to 10(-3) M of a single metal toxicant or combinations of metal toxicants for 12 hr in DME-F12 media. Slices were blotted and sandwiched between two mylar films stretched across XRF sample cups. Quantitation of the metal in the slices was performed by proton-induced X-ray emission analysis (PIXE). The uptake of the metals was rapid, often reaching a maximum between 3 to 6 hr; the accumulation of Hg was highest, followed in order by Cd, Cr, and As. When two metals were present together, substantial alterations were observed in the uptake of the metals in the slices. HgCl2 hindered the uptake of K2Cr2O7, NaAsO2, CdCl2 (in this order), whereas these metals facilitated the uptake of HgCl2. However, a decreased uptake of both metals was often noted after exposure to other combinations of metals. PIXE analysis of metal content in slices is attractive since all elements (atomic number > 20) can be determined simultaneously. This information will be particularly useful in studying potential toxic interactions.

Animals↗
PubMed1995

Antagonist and partial agonist actions of d-tubocurarine at mammalian muscle acetylcholine receptors.

Currents were elicited by acetylcholine (ACh), by d-tubocurarine (dTC), and by mixtures of ACh and dTC, from stably transformed fibroblasts that express fetal or adult muscle nicotinic receptors. dTC acted as an antagonist of ACh for activation of adult-type receptors, whereas it acted as a weak partial agonist at fetal-type receptors. The channel-blocking action of dTC was not apparent at the concentrations used. The partial agonism could explain previous observations that dTC is less effective at blocking the responses of fetal-type receptors than adult-type receptors. Binding of dTC to receptors was independently assayed by measuring the reduction of the initial rate of binding of iodinated alpha-bungarotoxin. Binding of dTC to the two types of receptor was indistinguishable. The dose-effect relationship for the interaction of dTC and ACh at fetal receptors is consistent with the affinities of dTC measured in binding experiments.

Acetylcholine↗
PubMed1995

[Effects of scopolamine on serotonin in the spinal cord and atria of morphine-dependent rats].

The effects of scopolamine on serotonin (5-HT) in the spinal cord and atria of morphine-dependent rats were studied. Levels of 5-HT and its metabolite, 5-hydroxyindolactic acid (5-HIAA) in the spinal cord and atria were analyzed by HPLC-ECD method. The results showed that contents of 5-HT, 5-HIAA in the spinal cord of morphine-dependent rats were statistically higher than those of controls (P < 0.01, n = 6), and that scopolamine inhibited morphine's effect by decreasing 5-HT, 5-HIAA in the spinal cord. After acute abstinence (1d), the contents of 5-HT in the spinal cord in natural withdrawal group were decreased, but increased in scopolamine group. After chronic abstinence (6d), the contents of 5-HT in the spinal cords in the two groups were all increased to above normal level. The results also showed that scopolamine did not affect the increasing of 5-HT in atria induced by morphine. The data support a role of muscarinic receptor on changes of 5-HT metabolism in the spinal cord in morphine-dependent rats.

Animals↗
PubMed1995

[Mesenteric vein thrombosis after devasculation for portal hypertension].

Six patients with mesenteric vein thrombosis (MVT) after devasculation for portal hypertension were treated by intestinal resection. Two patients had recurrence of thrombosis after the initial operations. Among 6 patients 2 survived and 4 (66.7%) died. MVT is an underappreciated, patentially lethal complication after revasculation. Three pathogenic factors after the operation may lead to thrombus formation of the portal vein, portal congestion, hypercoaguble state, and extensive ligation of portal branches. The complication commonly occurs in the recent period after devasculation. It is a characteristic manifestation of MVT that abdominal pain is out of proportion to physical findings. The most effective method is resection of infarcted bowel with sufficient length of normal bowel and its mesentery. In order to avoid a recurrence of thrombosis, postoperative anticoagulation treatment should be given.

Adult↗
PubMed1995

[Effect of scopolamine on morphine levels in serum and urine in rats].

Free morphine and conjugated morphine were determined by radioimmunoassay. Excretion of conjugated morphines in urine was increased significantly by treatment with scopolamine in a dose-related manner in morphine-dependent Sprague-Dawley rats (n = 8). Conjugated morphine in serum was increased by administration of scopolamine greater than that of controls at 2h, and both free and conjugated morphine in serum were enhanced at 24h after last injection of morphine in morphine-dependent rats (n = 6). After use of scopolamine (0.5mg/kg, bid, ip) for 3d the rats (n = 6) received single injection of morphine (10mg/kg, sc), the levels of free morphine were increased greater than those of controls at 2 and 10h. The data showed that scopolamine may not only induced the metabolism of morphine in liver, but also facilitated subcutaneous absorption of morphine, which result in enhancing the excretion of morphine.

Animals↗