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Biomedical subjects

Q Lin

Publications and source records attributed to Q Lin.

At least 127 records · Page 7Linked to original sources
PubMed1999

[Study on in vitro cytokines levels induced from peripheral mononuclear cells in patients with endometriosis].

OBJECTIVE: To study the changes and significance of interleukin-6 (IL-6), interleukin-8(IL-8), tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) levels in vitro cultured system of peripheral mononuclear cells in patient with endometriosis(Em). METHODS: Peripheral blood mononuclear cells from 31 cases of endometriosis, classified into mild group (stage I and II, n = 11), and severe group (stage III and IV, n = 20) according to the Revised American Fertility society criteria 1985, and 15 normal controls were separated and induced by lipopolysaccharide and phytohemagglutinin, followed by 48 hour incubation in vitro, then the supernatant were collected. The levels of IL-6, IL-8 and TNF-alpha were measured by enzyme linked immunosorbent assays, the concentrations of NO, expressed by nitrite and nitrate (NO2-/NO3-) content were measured by Griess methods. RESULTS: The concentrations of IL-6, IL-8, TNF-alpha and NO were significantly higher in both mild and severe Em groups than those in controls (P < 0.01). No differences between the mild and severe Em groups was seen. There were strong positive correlation between the levels of IL-6 and IL-8, TNF-alpha and NO in patients with endometriosis (P < 0.01). CONCLUSIONS: The immune function of peripheral mononuclear cell in patients with endometriosis was disordered. It may activate peripheral mononuclear cells to produce high levels of IL-6, IL-8, TNF-alpha and NO, which may take part in the pathogenesis of endometriosis.

Endometriosis↗
PubMed1999

Association of polymorphism of apolipoprotein E gene with coronary heart disease in Han Chinese.

OBJECTIVE: To investigate the association between apolipoprotein E (apoE) gene polymorphism and coronary heart disease(CHD) in Han Chinese. METHODS: Apo E genotype was examined with the methods of hot start polymerase chain reaction (PCR) and restriction isotyping in samples of 113 unrelated Chinese healthy individuals and 93 patients with CHD. The relation of the gene polymorphism of apoE and levels of serum lipids, lipoproteins, and apolipoproteins was also studied. RESULTS: The results showed that the epsilon 4/3 genotype was more frequent in CHD cases than in control subjects (31.2% vs. 11.5%, P < 0.01). The frequency of the epsilon 4 allele in CHD cases was significantly higher than in control subjects (17.2% vs 7.5%, P < 0.01). The epsilon 4 allele was associated with high concentrations of serum TC (r = 0.265, P < 0.05), LDL-C (r = 0.266, P < 0.05), and apoB (r = 0.360, P < 0.01). CONCLUSIONS: Hot start PCR assay is considered a rapid and simple technique for apoE genotyping. This method is suitable for routine laboratories and large scale population studies. Genetic polymorphism of the apoE gene might contribute to the determination of serum lipid profile and the development of CHD among Han Chinese.

Alleles↗
PubMed1999

[Studies on a G6PD polymorphic site, cDNA C1311T].

OBJECTIVE: To use amplification refractory mutation system(ARMS) method to detect the G6PD cDNA C1311T mutation, estimate its frequency in a normal south Chinese population, and investigate whether IVS-11 C93T mutation is the cause of certain G6PD deficient cases. METHODS: DNA sequencing was used to confirm the C1311T and the IVS-11 C93T mutations. ARMS was set up to detect the C1311T and to estimate its frequency. RESULTS: Three cases of C1311T mutation were found in 40 G6PD deficient samples. The optimal condition for ARMS was established. Using this method, 19 cases of C1311T were detected in 103 normal men, and the frequency of this polymorphic mutation was estimated to be 18.4% in southern Chinese population. Four cases with G6PD deficiency were demonstrated to be C at the IVS-11 93 position. At the same time, a case of IVS-11 93 C-->T was found in a normal man. CONCLUSIONS: ARMS is a simple, time-saving, and reliable method for detecting known G6PD gene point mutation. The frequency of C1311T in a normal south Chinese population is 18.4%. IVS-11 C93T might be another polymorphic site of the G6PD gene, and it is not the cause of enzyme deficiency in certain G6PD deficient cases.

Asian People↗
PubMed1999

[A case-control study on cerebral palsy in children].

OBJECTIVE: To identify the risk factors for cerebral palsy (CP) in children. METHODS: A population-based 1:2 matched case-control study was conducted during May to June 1997 in southern Jiangsu Province of China. RESULTS: Risk factors for CP in children could be summarized into four categories, i.e.; (1) fetal growth retardation, preterm delivery and low birth weight; (2) asphyxia at birth, intracranial hemorrhage, ischemic and hypoxic encephalopathy and hyperbilirubinemic encephalopathy; (3) delivery with vaccum suction and traumatic brain injury; and (4) other prenatal factors. CONCLUSION: The first and second categories of risk factors correlated strongly and reproducibly with CP in children. It is emphasized that antenatal care be enforced to prevent occurrence of risk factors, such as low birth weight, etc., and the newborns with asphyxia be vigorously rescued and put under close supervision. For risk factors in the third category, the key measures should be obstetric practice and health education for the parents. But, little about the knowledge of the risk factors in the fourth category has been understood, which could be associated with those in the first two categories.

Asphyxia Neonatorum↗
PubMed1999

[Relationship of nitric oxide and immunal function of the patients with acute hepatitis and hepatic cirrhosis].

The interleukin-12(IL-12), interleukin-10(IL-10), tumor necrosis factor(TNF) and nitric oxide (NO) levels in serum of 90 patients with hepatitis and cirrhosis were measured by the method of ELISA and colorimeter. The levels of IL-12, IL-10 and NO in serum of the patients with hepatitis were in close proximity to the level of healthy control, but the TNF level was significantly higher than that of healthy control. The IL-12, IL-10, TNF and NO levels in serum of the patients of hepatic cirrhosis were significantly higher than that of healthy control and patients with hepatitis. The results suggested that the NO level was not related with the hepatic damage of acute hepatitis. The dysfunction of immunology in the patients with cirrhosis was related with the increase of NO level.

Adult↗
PubMed1999

[Polymorphism at cholesteryl ester transfer protein gene loci in patients with gallstone].

This study was designed to reveal the association between the polymorphism of cholesteryl ester transfer protein (CETP) gene loci and gallbladder stone disease. By means of polymerase chain reaction (PCR) and restriction fragment length polymorphisms (RFLEs) of CETP taqIB, BamHI genes were examined in 104 patients subjected to cholecystectomy for symptomatic gallstone disease and 68 healthy controls. The distribution of CETP taqIB polymorphism in the patients with gallstones differed significantly from that of the controls. The B1 allele and B1B1 jects were more frequently revealed in patients with gallstones (0.523, vs 0.346, 0.288 vs 0.1176, P < 0.05). The B2 allele and the B2B2 jects appeared in the controls more frequently (0.654 vs 0.477, 0.4264 vs 0.242, P < 0.05). The H1 allele, H2 allele and H1H1 genotypic, H2H2 genotypic frequencies of the patients with gallstones were not significantly different from those of the controls (P > 0.05). The results suggest that B1 allele is the major gene in the patients with gallstones, and B2 allele is more frequently revealed in the controls.

Adult↗
PubMed1999

[Experimental study on antiendotoxin effect of extracts from Artemisia annua L].

OBJECTIVE: To explore the antiendotoxin effect of extracts from Artemisia annua (AA) and qinghaosu (QHS). METHOD: LPO and SOD in chondriosome, ACP in lysosomes, tumor nicrosis factor-alpha(TNF-alpha) and endotoxin in plasma, and P450 concentration in hepatic microsome of rats were determined. Mortality of endotoxemic mice and histomorphology were observed. RESULT: LPO, ACP, endotoxin, TNF-alpha and P450 content were decreased with AA and QHS. SOD activity was increased with AA and QHS. At the same time, mortality was decreased. Histomorphology of lysosomes and chondriosome of rats were protected from endotoxin. CONCLUSION: AA and QHS possess an antiendotoxin effect.

Animals↗
PubMed1998

A constitutive mutation of ALK5 disrupts cardiac looping and morphogenesis in mice.

TGF beta family members are implicated in cardiac organogenesis, growth control, and positional information, including the direction of cardiac looping. However, genetic analysis of TGF beta signaling in mice has been confounded, in some cases, by noncardiac and generalized defects. Hence, deciphering TGF beta function in myocardium would benefit from cardiac-restricted mutations. We developed a constitutively activated type I receptor, ALK5L193A,P194A,T204D, and directed it to embryonic myocardium in transgenic mice. Expression of the activated ALK5 gene arrests looping morphogenesis and causes a linear, dilated, hypoplastic heart tube, despite normal expression of Nkx2.5 and dHAND, cardiogenic transcription factors whose absence provokes a similar phenotype. Ventricular hypoplasia was associated with precocious induction of the cyclin-dependent kinase inhibitor, p21. Thus, an ALK5-sensitive pathway mediates looping, perhaps through control of cardiac myocyte proliferation.

Activin Receptors, Type I↗
PubMed1998

T and B cell development in BP-1/6C3/aminopeptidase A-deficient mice.

Stage-restricted expression of cell surface molecules serves to delineate B lineage cells during their progressive differentiation within the bone marrow. The BP-1/6C3 Ag, aminopeptidase A (APA), is selectively expressed by the pre-B and immature B cells. This ectoenzyme, which is also present on bone marrow-derived stromal cells, thymic cortical epithelial cells, renal proximal tubular cells, intestinal enterocytes, and endothelial cells, cleaves acidic glutamyl and aspartyl residues from the N-terminus of angiotensin and other biologically active peptides to quench their functional activity. BP-1/6C3/APA expression by early B lineage cells is up-regulated by IL-7, an important growth factor for pre-B cells and T cells. To explore the physiologic role of this peptidase, we generated a mouse model of BP-1 deficiency by gene targeting in embryonal stem cells. While mice homozygous for the BP-1 mutation did not express detectable BP-1 protein or enzyme activity, they developed normally, generated normal numbers of T and B cells, exhibited integrity of Ab responses to both thymus-dependent and -independent Ags, and produced normal serum Ig levels. Phenotypic analysis of bone marrow and thymic lymphocytes indicated a normal pattern of B and T lineage differentiation. B lymphopoiesis in fetal liver cultures and the proliferative responses of bone marrow cells to IL-7 and LPS were also unimpaired. These findings indicate that BP-1 ectoenzyme activity is not essential for normal B and T cell development.

Aminopeptidases↗
PubMed1998

Overlapping roles and asymmetrical cross-regulation of the USF proteins in mice.

USF1 and USF2 are ubiquitously expressed transcription factors implicated as antagonists of the c-Myc protooncoprotein in the control of cellular proliferation. To determine the biological role of the USF proteins, mutant mice were generated by homologous recombination in embryonic stem cells. USF1-null mice were viable and fertile, with only slight behavioral abnormalities. However, these mice contained elevated levels of USF2, which may compensate for the absence of USF1. In contrast, USF2-null mice contained reduced levels of USF1 and displayed an obvious growth defect: they were 20-40% smaller at birth than their wild-type or heterozygous littermates and maintained a smaller size with proportionate features throughout postnatal development. Some of the USF-deficient mice, especially among the females, were prone to spontaneous epileptic seizures, suggesting that USF is important in normal brain function. Among the double mutants, an embryonic lethal phenotype was observed for mice that were homozygous for the Usf2 mutation and either heterozygous or homozygous for the Usf1 mutation, demonstrating that the USF proteins are essential in embryonic development.

Alleles↗
PubMed1998

Nitric oxide contributes to central sensitization following intradermal injection of capsaicin.

This study provides direct evidence from measurements of its metabolites, NO2- and NO3-, that NO is released in the spinal cord during central sensitization. A microdialysis fiber was implanted in the dorsal horn at L5 for collecting dialysate and administering drugs. Dialysate was pumped through a cadminum reducing column, a post-column derivatizing unit, and then a u.v. detector. After injection of capsaicin into one hind foot, NO2-increased in the dialysate. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME) significantly reduced NO release induced by a second injection of capsaicin into the opposite foot. This supports the ideas that NO is involved in central sensitization in the spinal cord and contributes to hyperalgesia and allodynia following capsaicin injection.

Analysis of Variance↗
PubMed1998

Alterations in NF-kappaB function in transgenic epithelial tissue demonstrate a growth inhibitory role for NF-kappaB.

Stratified epithelium contains a mitotically active basal layer of cells that cease proliferating, then migrate outwards and undergo terminal differentiation. The control of this process, which is abnormal in cutaneous neoplasia and inflammation, is not well understood. In normal epidermis, NF-kappaB proteins were found to exist in the cytoplasm of basal cells and then to localize in the nuclei of suprabasal cells, suggesting a role for NF-kappaB in the switch from proliferation to growth arrest and differentiation. Functional blockade of NF-kappaB by expressing dominant-negative NF-kappaB inhibitory proteins in transgenic murine and human epidermis produced hyperplastic epithelium in vivo. Consistent with this, application of a pharmacologic inhibitor of NF-kappaB to intact skin induced epidermal hyperplasia. In contrast, overexpression of active p50 and p65 NF-kappaB subunits in transgenic epithelium produced hypoplasia and growth inhibition. These data suggest that spatially restricted NF-kappaB activation occurs in stratified epithelium and indicate that NF-kappaB activation in this tissue, in contrast to its role in other settings, is important for cellular growth inhibition.

Animals↗
PubMed1998

[p16INK4/CDKN2 gene deletions and mutations in non-small cell lung cancers].

OBJECTIVE: To investigate the genomic status of cyclindependent kinase-4 inhibitor, p16 INK4/CDKN2 gene in primary non-small cell lung cancers. METHODS: p16 gene was analysed by duplex PCR, PCR-SSCP, and sequencing in 31 primary non-small cell lung cancer (NSCLC) tissues. RESULTS: Gene deletions were found in three samples (3/31), one case had whole p16 gene deletion and the other two had deletion in exon 1 and in exon 2 respectively. Two cases of point mutations (2/30) in the gene had been found, one in exon 1 and another one in exon 2. In the 5 cases of p16 gene abnormal samples, 4 cases (two cases of deletions and two cases of mutations) were non-small cell lung cancers with lymphnode metastasis (4/20). CONCLUSION: These results indicate that inactivation of p16 gene is associated with some NSCLC (5/31), and probably be a late event in NSCLC carcinogenesis.

Adult↗
PubMed1998

Impairment of T and B cell development by treatment with a type I interferon.

Type I interferons alpha and beta, naturally produced regulators of cell growth and differentiation, have been shown to inhibit IL-7-induced growth and survival of B cell precursors in vitro. After confirming an inhibitory effect on B lymphopoiesis in an ex vivo assay, we treated newborn mice with an active IFN-alpha2/alpha1 hybrid molecule to assess its potential for regulating B and T cell development in vivo. Bone marrow and splenic cellularity was greatly reduced in the IFN-alpha2/alpha1-treated mice, and B lineage cells were reduced by >80%. The bone marrow progenitor population of CD43+B220+HSA- cells was unaffected, but development of the CD19+ pro-B cells and their B lineage progeny was severely impaired. Correspondingly, IL-7-responsive cells in the bone marrow were virtually eliminated by the interferon treatment. Thymus cellularity was also reduced by >80% in the treated mice. Phenotypic analysis of the residual thymocytes indicated that the inhibitory effect was exerted during the pro-T cell stage in differentiation. In IFN-alpha/beta receptor-/- mice, T and B cell development were unaffected by the IFN-alpha2/alpha1 treatment. The data suggest that type I interferons can reversibly inhibit early T and B cell development by opposing the essential IL-7 response.

Animals↗
PubMed1998

Protein surface recognition by synthetic agents: design and structural requirements of a family of artificial receptors that bind to cytochrome c.

The design, synthesis, and evaluation of a novel series of receptors for protein surface recognition are described. The design of these agents is based around the attachment of four constrained peptide loops onto a central calix[4]arene scaffold. This arrangement mimics the role of the hypervariable loops in antibody combining regions and defines a large surface area for binding to a complementary region of the exterior of a target protein. Using affinity and gel filtration chromatographies we show that one particular receptor binds strongly to the surface of cytochrome c. The site of binding is presumably close to the heme edge region, which contains several charged lysine residues. This is supported by the observation that the receptor inhibits the reduction of Fe(III) cytochrome c to its Fe(II) form. We also show that binding is strongly dependent on the nature of the substituents on the lower rim of the calixarene. The nmr and computational studies suggest that this effect may be due to conformational differences among the differently substituted receptors.

Animals↗
PubMed1998

Behavioral and cellular protection of rat dopaminergic neurons by an adenoviral vector encoding glial cell line-derived neurotrophic factor.

Previously, we observed that an adenoviral (Ad) vector encoding human glial cell line-derived neurotrophic factor (GDNF), injected near the rat substantia nigra (SN), protects SN dopaminergic (DA) neuronal soma from 6-hydroxydopamine (6-OHDA)-induced degeneration. In the present study, the effects of Ad GDNF injected into the striatum, the site of DA nerve terminals, were assessed in the same lesion model. So that effects on cell survival could be assessed without relying on DA phenotypic markers, fluorogold (FG) was infused bilaterally into striatae to retrogradely label DA neurons. Ad GDNF or control treatment (Ad mGDNF, encoding a deletion mutant GDNF, Ad lacZ, vehicle, or no injection) was injected unilaterally into the striatum near one FG site. Progressive degeneration of DA neurons was initiated 7 days later by unilateral injection of 6-OHDA at this FG site. At 42 days after 6-OHDA, Ad GDNF prevented the death of 40% of susceptible DA neurons that projected to the lesion site. Ad GDNF prevented the development of behavioral asymmetries which depend on striatal dopamine, including limb use asymmetries during spontaneous movements along vertical surfaces and amphetamine-induced rotation. Both behavioral asymmetries were exhibited by control-treated, lesioned rats. Interestingly, these behavioral protections occurred in the absence of an increase in the density of DA nerve fibers in the striatum of Ad GDNF-treated rats. ELISA measurements of transgene proteins showed that nanogram quantities of GDNF and lacZ transgene were present in the striatum for 7 weeks, and picogram quantities of GDNF in the SN due to retrograde transport of vector and/or transgene protein. These studies demonstrate that Ad GDNF can sustain increased levels of biosynthesized GDNF in the terminal region of DA neurons for at least 7 weeks and that this GDNF slows the degeneration of DA neurons and prevents the appearance of dopamine dependent motor asymmetries in a rat model of Parkinson's disease (PD). GDNF gene therapy targeted to the striatum, a more surgically accessible site than the SN, may be clinically applicable to humans with PD.

Adenoviridae↗