Biomedical subjects

Hong Lin

Publications and source records attributed to Hong Lin.

At least 37 records · Page 2Linked to original sources

PubMed2005

Tissue Doppler echocardiographic evidence of atrial mechanical dysfunction in coronary artery disease.

BACKGROUND: Atrial function is an integral part of cardiac function which is often neglected. The presence of coronary artery disease (CAD) may impair atrial function. This study investigated if atrial mechanical dysfunction was present in patients with CAD by tissue Doppler echocardiography (TDI). METHODS: Echocardiography with TDI was performed in 118 patients with CAD, and compared with 100 normal controls with comparable age and heart rate. Regional atrial function was assessed at the left (LA) and right (RA) atrial free wall and inter-atrial septum (IAS). The peak regional atrial contraction velocity of (V(A)) and the timing of mechanical events were compared. RESULTS: The V(A) in the LA (5.0+/-2.6 Vs 7.7+/-2.6 cm/s), IAS (4.8+/-1.7 Vs 5.7+/-1.5 cm/s) and RA (6.8+/-3.1 Vs 9.2+/-2.9 cm/s) were significantly decreased in patients with CAD when compared with controls (all p<0.001). Patients with impaired systolic function (ejection fraction 50% (both p<0.001); and were lower in those with restrictive filling pattern (RFP) than non-RFP of diastolic dysfunction (both p<0.05). The V(A) in all the subgroups was lower than controls. In contrast, transmitral atrial velocity was unable to reveal any abnormality except in the subgroup with a RFP. The LA dimension, area and volume were increased in the disease groups, but were largely unchanged in the RA despite abnormal V(A). The physiological inter-atrial delay for the onset and peak atrial contraction between the RA and LA were unaffected by CAD. CONCLUSIONS: The atrial contractile function in both atria was impaired in the presence of CAD, especially in the LA. This was detected even in patients with preserved systolic function or mild diastolic dysfunction such as non-RFP. Direct assessment of atrial velocity by TDI may better reflect atrial mechanical function than transmitral atrial velocity.

Atrial Function, Right↗

PubMed2005

RNA-binding protein is involved in aggregation of light neurofilament protein and is implicated in the pathogenesis of motor neuron degeneration.

Abnormal protein aggregation is emerging as a common theme in the pathogenesis of neurodegenerative disease. Our previous studies have shown that overexpression of untranslated light neurofilament (NF-L) RNA causes motor neuron degeneration in transgenic mice, leads to accumulation of ubiquitinated aggregates in degenerating cultured motor neurons and triggers aggregation of NF-L protein and co-aggregation of mutant SOD1 protein in neuronal cells. Here, we report that p190RhoGEF, an RNA-binding protein that binds to a destabilizing element in NF-L mRNA, is involved in aggregation of NF-L protein and is implicated in the pathogenesis of motor neuron degeneration. We show that p190RhoGEF co-aggregates with unassembled NF-L protein and that co-aggregation is associated with down-regulation of parent NF-L mRNA in neuronal cells. Co-expression of NF-M increases NF assembly and reduces RNA-triggered aggregation as well as loss of solubility of NF-L protein. siRNA-induced down-regulation of p190RhoGEF not only reduces aggregation and promotes assembly of NF-L and NF-M, but also causes reversal of aggregation and recovery of NF assembly in transfected cells. Examination of transgenic models of motor neuron disease shows that prominent aggregates of p190RhoGEF and NF-L and down-regulation of NF-L expression occur in degenerating motor neurons of mice expressing untranslated NF-L RNA or a G93A mutant SOD1 transgene. Moreover, aggregates of p190RhoGEF and NF-L appear as early pathological changes in presymptomatic G93A mutant SOD1 transgenic mice. Together, the findings indicate that p190RhoGEF is involved in aggregation of NF-L protein and support a working hypothesis that aggregation of p190RhoGEF and NF-L is an upstream event triggering neurotoxicity in motor neuron disease.

Animals↗

PubMed2005

Investigation of cooperativity in the binding of ligands to the D(2) dopamine receptor.

The D(2) dopamine receptor exists as dimers or as higher-order oligomers, as determined from data from physical experiments. In this study, we sought evidence that this oligomerization leads to cooperativity by examining the binding of three radioligands ([(3)H]nemonapride, [(3)H]raclopride, and [(3)H]spiperone) to D(2) dopamine receptors expressed in membranes of Sf9 cells. In saturation binding experiments, the three radioligands exhibited different B(max) values, and the B(max) values could be altered by the addition of sodium ions to assays. Despite labeling different numbers of sites, the different ligands were able to achieve full inhibition in competition experiments. Some ligand pairs also exhibited complex inhibition curves in these experiments. In radioligand dissociation experiments, the rate of dissociation of [(3)H]nemonapride or [(3)H]spiperone depended on the sodium ion concentration but was independent of the competing ligand. Although some of the data in this study are consistent with the behavior of a cooperative oligomeric receptor, not all of the data are in agreement with this model. It may, therefore, be necessary to consider more complex models for the behavior of this receptor.

Animals↗

PubMed2005

NOS-positive local circuit neurons are exclusively axo-dendritic cells both in the neo- and archi-cortex of the rat brain.

Neuronal nitric oxide synthase (nNOS)-containing neurons and axon terminals were examined in the rat somatosensory and temporal neocortex, in the CA3/a-c areas of Ammon's horn and in the hippocampal dentate gyrus. In these areas, only nonpyramidal neurons were labeled with the antibody against nNOS. Previous observations suggested that all nNOS-positive nonpyramidal cells are GABAergic local circuit neurons, which form exclusively symmetric synapses. In agreement with this, nNOS-positive axon terminals in the hippocampal formation formed symmetric synapses exclusively with dendritic shafts. In the neocortex, in contrast, in addition to the nNOS-positive axon terminals that formed synapses with unlabeled spiny and aspiny dendrites and with nNOS-positive aspiny dendrites, a small proportion of the nNOS-positive axon terminals formed symmetric synapses with dendritic spines. These results suggest that nNOS-positive local circuit neurons form a distinct group of axo-dendritic cells displaying slightly different domain specificity in the archi- and neocortex. However, nNOS-positive cells show no target selectivity, because they innervate principal cells and local circuit neurons. Afferents to the NOS-positive cells display neither domain nor target selectivity, because small unlabeled terminals formed synapses with both the soma or dendrites of nNOS-positive neurons and an adjacent unlabeled dendrite or spine in both the hippocampal formation and in neocortex.

Animals↗

PubMed2005

HoxB2 binds mutant SOD1 and is altered in transgenic model of ALS.

Mutations in Cu/Zn superoxide dismutase (SOD1) cause approximately 20% of familial amyotrophic lateral sclerosis by a toxic gain of function; however, the precise mechanisms remain unclear. Here, we report the identification of HoxB2, a homeodomain-containing transcription factor, as a G93A mutant SOD1 interactive protein in a yeast two-hybrid screen. We show that HoxB2 co-precipitates and co-localizes with mutant SOD1 in neuronal cell lines, as well as in brain and spinal cord of G93A mutant SOD1 transgenic mice. Mutagenesis further shows that this interaction is mediated by the central homeodomain of HoxB2. In motor neuron-like NSC-34 cells, overexpression of HoxB2 or its homeodomain decreases the insolubility of mutant SOD1 and inhibits G93A or G86R mutant SOD1-induced neuronal cell death. In human and mouse tissues, we show that expression of HoxB2 persists in adult spinal cord and is primarily localized in nuclei of motor neurons. In G93A transgenic mice, HoxB2 co-localizes with mutant SOD1 and is redistributed to perikarya and proximal neurites of motor neurons. In addition, there is progressive accumulation of HoxB2 and mutant SOD1 as punctate inclusions in the neuropil surrounding motor neurons. Taken together, our findings demonstrate that interaction of HoxB2 with mutant SOD1 occurs in motor neurons of G93A mutant SOD1 transgenic mice and suggest that this interaction may modulate the neurotoxicity of mutant SOD1.

Amyotrophic Lateral Sclerosis↗

PubMed2005

The role of epidermal growth factor receptor in ethanol-mediated inhibition of activator protein-1 transactivation.

A potential mechanism underlying ethanol-induced alterations in gene expression is the disruption of transcription factor activity. Growth factor receptors, particularly receptor tyrosine kinases, play an important role in modulating many biological effects of ethanol. We demonstrated here that the expression of epidermal growth factor receptor (EGFR) mediated the effect of ethanol on the activity of transcription factor activator protein-1 (AP-1). Ethanol had little effect on AP-1 activity in the fibroblast cells devoid of EGFR (B82); however, it significantly suppressed AP-1 activity in B82 cells that were stably transfected with either a wild-type EGFR (B82L) or a kinase-deficient receptor (B82M721) in a concentration-dependent manner. EGF activated AP-1 only in B82L cells; the activation was mediated primarily by Akt and ERK. Ethanol inhibited EGF-induced EGFR autophosphorylation, phosphorylation of ERK as well as Akt and its substrate GSK-3beta, and subsequently blocked EGF-stimulated AP-1 activation in B82L cells. On the other hand, ethanol had little effect on EGF-stimulated JNK activation. Phorbol ester 12-O-teradecanoyl-phorbol-13-acetate (TPA) activated AP-1 in B82L and B82M721 cells, but not B82 cells. TPA-induced activation of ERK and PKCdelta was dependent on the expression of EGFR although the intrinsic kinase activity of EGFR was not required. In contrast, TPA-induced phosphorylation of p38 MAPK, JNKs and other PKC isoforms was independent of EGFR. Ethanol selectively inhibited TPA-induced phosphorylation of ERK and PKCdelta, and modestly suppressed TPA-stimulated AP-1 activation in B82L and B82M721 cells. Thus, EGFR plays a critical role in the interaction between ethanol and AP-1.

Animals↗

PubMed2005

A novel tool to assess systolic asynchrony and identify responders of cardiac resynchronization therapy by tissue synchronization imaging.

OBJECTIVES: This study was designed to investigate if tissue synchronization imaging (TSI) is useful to identify regional wall delay and predict left ventricular (LV) reverse remodeling after cardiac resynchronization therapy (CRT). BACKGROUND: Echocardiographic assessment of systolic asynchrony is helpful to predict a positive response to CRT. Tissue synchronization imaging is a new imaging technique that allows quick evaluation of regional systolic delay. METHODS: Tissue synchronization imaging was performed in 56 heart failure patients at baseline and three months after CRT. Regional wall delay was identified on TSI images and the time to regional peak systolic velocity (Ts) in LV was measured by the six-basal-six-mid-segmental model. Eight TSI parameters of systolic asynchrony were computed when Ts was measured in ejection phase or also included postsystolic shortening. RESULTS: Severe lateral wall delay occurred in 17 patients, which predicted LV reverse remodeling (chi-square = 8.13, p = 0.004). Among the eight quantitative parameters of asynchrony, the predictive values were higher for parameters that measured Ts in ejection phase than in postsystolic shortening. The standard deviation of Ts of 12 LV segments in ejection phase (Ts-SD-12-ejection) was most powerful to predict reverse remodeling (r = -0.61, p < 0.001) and gain in ejection fraction (r = 0.53, p < 0.001). The area of the receiver-operating characteristic (ROC) curve was the largest for Ts-SD-12-ejection (0.90, p < 0.001), with a sensitivity of 87% and specificity of 81% at a cutoff of 34.4 ms. The combination of lateral wall delay with Ts-SD-12-ejection gave a sensitivity and specificity of 82% and 87%. CONCLUSIONS: Tissue synchronization imaging allows quick evaluation of regional wall delay, and combined with Ts-SD-12-ejection provides a reliable way of predicting reverse remodeling after CRT.

Aged↗

PubMed2005

Multilocus simple sequence repeat markers for differentiating strains and evaluating genetic diversity of Xylella fastidiosa.

A genome-wide search was performed to identify simple sequence repeat (SSR) loci among the available sequence databases from four strains of Xylella fastidiosa (strains causing Pierce's disease, citrus variegated chlorosis, almond leaf scorch, and oleander leaf scorch). Thirty-four SSR loci were selected for SSR primer design and were validated in PCR experiments. These multilocus SSR primers, distributed across the X. fastidiosa genome, clearly differentiated and clustered X. fastidiosa strains collected from grape, almond, citrus, and oleander. They are well suited for differentiating strains and studying X. fastidiosa epidemiology and population genetics.

Base Sequence↗

PubMed2005

[Evaluation of therapeutic effect of acupuncture at Jiaji (EX-B 2) on hyperosteogeny of lumbar vertebrae].

OBJECTIVE: To assess therapeutic effect of acupuncture at Jiaji (EX-B 2) on hyperosteogeny of lumbar vertebrae. METHODS: Seventy-two cases were treated with Huatuo jiaji (EX-B 2) of L2 approximately L5 as main acupoints, and their clinical therapeutic effects were assessed with Oswestry Disability Index (ODI). RESULTS: ODI was 0.562 +/- 0.199 before treatment and 0.123 +/- 0.196 after treatment with a significant difference before and after treatment (P<0.01), and the effective rate was 94.4%. CONCLUSION: Acupuncture at Jiaji (EX-B 2) can improve functional activity for the patient of hyperosteogeny of lumbar vertebrae.

Acupuncture Points↗

PubMed2005

[Observation on therapeutic effect of combination of acupuncture with drug on depression].

OBJECTIVE: To assess clinical therapeutic effect and safety of acupuncture combined with fuxiting on depression. METHODS: Fifty-three cases of depression were divided into an observation group (n = 30) treated by acupuncture combined with fuxiting and a control group treated by fuxiting. Their clinical therapeutic effects were assessed by HAMD, HAMA and CGI, and adverse effects by TESS. RESULTS: After treatment of 6 weeks, the total effective rate was 80.0% in the observation group and 69.6% in the control group with no significant difference between the two groups (P > 0.05). There were significant differences in scores of HAMD and HAMA before and after treatment in the two groups (P < 0.01), with no significant difference between the two groups (P > 0.05). The adverse effect in the observation group was less and milder than that in the control group. CONCLUSION: Acupuncture combined fuxiting has good therapeutic effect on depression with less and mild adverse effects.

Acupuncture Therapy↗

PubMed2004

Ethanol-induced in vitro invasion of breast cancer cells: the contribution of MMP-2 by fibroblasts.

Ethanol is a tumor promoter and may promote metastasis of breast cancer. However, the underlying cellular/molecular mechanisms remain unknown. Overexpression and high activity of matrix metalloproteinase-2 (MMP-2) are frequently associated with metastatic breast cancers and serve as a prognostic indicator of clinical outcome. MMP-2 is predominantly expressed in stromal fibroblasts and plays a pivotal role in regulating the invasive behavior of breast tumor cells. We hypothesized that ethanol may enhance the invasion of breast tumor cells by modulating the activity of fibroblastic MMP-2. With in vitro models (HS68 and CCD1056SK human fibroblasts), we showed that ethanol at physiologically relevant concentrations (50-200 mg/dl) activated MMP-2; conversely, at a higher concentration (400 mg/dl), it inhibited the MMP-2 activity. Consistently, conditioned medium collected from ethanol (50-200 mg/dl)-exposed fibroblasts markedly enhanced the invasive potential of breast cancer cells and mammary epithelial cells overexpressing ErbB2/HER2 (BT474, SKBR-3 and HB2(ErbB2) cells) but had little effect on cells with low ErbB2 levels (BT20 and HB2 cells). In contrast, conditioned medium obtained from ethanol (400 mg/dl)-treated fibroblasts inhibited cell invasion. Selective inhibitors of MMP-2 (SB-3CT and OA-Hy) eliminated ethanol-stimulated invasion, indicating that the effect of ethanol was mediated by MMP-2. Ethanol activated conventional PKCs and JNKs in fibroblasts; inhibitors of PKC (Go6850 and Go6976) and JNKs (SP600125) significantly inhibited ethanol-mediated MMP-2 activation as well as cell invasion, indicating that PKCs and JNKs play a role in ethanol-induced MMP-2 activation and cell invasion in vitro. Thus, ethanol-promoted breast cancer cell invasion may be mediated by the modulation of fibroblastic MMP-2.

Biological Assay↗

PubMed2004

Mechanisms of agonist action at D2 dopamine receptors.

In this study, we investigated the biochemical mechanisms of agonist action at the G protein-coupled D2 dopamine receptor expressed in Chinese hamster ovary cells. Stimulation of guanosine 5'-O-(3-[35S]thio)triphosphate ([35S]GTPgammaS) binding by full and partial agonists was determined at different concentrations of [35S]GTPgammaS (0.1 and 10 nM) and in the presence of different concentrations of GDP. At both concentrations of [35S]GTPgammaS, increasing GDP decreased the [35S]GTPgammaS binding observed with maximally stimulating concentrations of agonist, with partial agonists exhibiting greater sensitivity to the effects of GDP than full agonists. The relative efficacy of partial agonists was greater at the lower GDP concentrations. Concentration-response experiments were performed for a range of agonists at the two [35S]GTPgammaS concentrations and with different concentrations of GDP. At 0.1 nM [35S]GTPgammaS, the potency of both full and partial agonists was dependent on the GDP concentration in the assays. At 10 nM [35S]GTPgammaS, the potency of full agonists exhibited a greater dependence on the GDP concentration, whereas the potency of partial agonists was virtually independent of GDP. We concluded that at the lower [35S]GTPgammaS concentration, the rate-determining step in G protein activation is the binding of [35S]GTPgammaS to the G protein. At the higher [35S]GTPgammaS concentration, for full agonists, [35S]GTPgammaS binding remains the slowest step, whereas for partial agonists, another (GDP-independent) step, probably ternary complex breakdown, becomes rate-determining.

Animals↗

PubMed2004

Tissue Doppler imaging is superior to strain rate imaging and postsystolic shortening on the prediction of reverse remodeling in both ischemic and nonischemic heart failure after cardiac resynchronization therapy.

BACKGROUND: A number of noninvasive techniques have been used to predict the effectiveness of cardiac resynchronization therapy (CRT) in heart failure patients, in particular left ventricular (LV) reverse remodeling. This study compared the relative predictive values of tissue Doppler imaging (TDI) and strain-rate imaging (SRI) parameters for LV reverse remodeling in patients who received CRT and examined for potential differences in ischemic (n=22) and nonischemic (n=32) heart failure. METHODS AND RESULTS: TDI and SRI were performed at baseline and 3-month follow-up. Eighteen parameters of intraventricular and interventricular asynchrony based on the time to peak myocardial contraction (Ts) and time to peak strain rate (Tsr) were compared, along with postsystolic shortening (PSS). Reverse remodeling with reduction of LV end-diastolic and end-systolic volumes and gain in ejection fraction (all P<0.001) was observed in the whole study population. The standard deviation of Ts of 12 LV segments (Ts-SD) is the most powerful predictor of reverse remodeling in both the ischemic (r=-0.65, P<0.001) and nonischemic (r=-0.79, P<0.001) groups. The PSS of 12 LV segments was a good predictor only for the nonischemic (r=-0.64, P<0.001) but not the ischemic (r=0.32, P=NS) group. However, parameters of SRI and interventricular asynchrony failed to predict reverse remodeling. By multiple regression analysis, independent parameters included Ts-SD in both groups (P<0.005) and PSS of 12 LV segments in the nonischemic group (P=0.03). The area of the receiver operating characteristic curve was largest for Ts-SD (0.94; CI=0.88 to 1.00). CONCLUSIONS: Ts-SD is the most powerful predictor of LV reverse remodeling and was consistently useful for ischemic and nonischemic heart failure. However, PSS is useful only for nonischemic pathogenesis, whereas the role of SRI parameters was not supported by the present study.

Aged↗

PubMed2004

[Quality control of clinical-grade recombinant adenovirus used in gene therapy].

OBJECTIVE: To establish the quality control methods and reference standards for clinical-grade recombinant adenovirus products for human gene therapy. METHODS: The Infectivity of clinical grade recombinant adenoviral vectors is determined by a TCID(50) assay. The purity is determined by a high-performance liquid chromatography (HPLC) assay. A549 cells were used in replication competent adenovirus (RCA) assay of samples by observation of the cytopathic effect. Other quality control assays were performed in accordance with the SFDA Regulations for Biological Products. RESULTS: The recombinant adenovirus encoding human p53 gene produced at SiBiono (Lot 20010701) has the following quality attributes: viral particle concentration: 1.03 (10(12) VP/ml, infectivity titer: 5.01 (10(10) IU/ml, specific infectivity (IU/VP): 4.86%, higher than the 3.3% required by the Food and Drug Administration (FDA), USA; Purity by HPLC analysis: 98.62%, higher than the 95% purity specified by SFDA; and level of RCA: less than 1 RCA/3 (10(10) VP, meeting the standards established by SFDA. CONCLUSIONS: A whole set of quality standards of clinical-grade recombinant adenovirus vectors has been established so as to ensure the clinical safety and efficacy of recombinant adenoviral vectors for human gene therapy.

Adenoviridae↗

PubMed2004

Investigation of the mechanism of agonist and inverse agonist action at D2 dopamine receptors.

This study investigated, for the D2 dopamine receptor, the relation between the ability of agonists and inverse agonists to stabilise different states of the receptor and their relative efficacies. Ki values for agonists were determined in competition versus the binding of the antagonist [3H]spiperone. Competition data were fitted best by a two-binding site model (with the exception of bromocriptine, for which a one-binding site model provided the best fit) and agonist affinities for the higher (Kh) (G protein-coupled) and lower affinity (Kl) (G protein-uncoupled) sites determined. Ki values for agonists were also determined in competition versus the binding of the agonist [3H]N-propylnorapomorphine (NPA) to provide a second estimate of Kh. Maximal agonist effects (Emax) and their potencies (EC50) were determined from concentration-response curves for agonist stimulation of guanosine-5'-O-(3-[32S]thiotriphosphate) ([35S]GTPgammaS) binding. The ability of agonists to stabilise the G protein-coupled state of the receptor (Kl/Kh determined from ligand-binding assays) did not correlate with either of two measures of relative efficacy (relative Emax, Kl/EC50) of agonists determined in [35S]GTPgammaS-binding assays, when the data for all of the compounds tested were analysed. For a subset of compounds, however, there was a relation between Kl/Kh and Emax. Competition-binding data versus [3H]spiperone and [3H]NPA for a range of inverse agonists were fitted best by a one-binding site model. Ki values for the inverse agonists tested were slightly lower in competition versus [3H]NPA compared to [3H]spiperone. These data do not provide support for the idea that inverse agonists act by binding preferentially to the ground state of the receptor.

Animals↗

PubMed2004

3' untranslated region in a light neurofilament (NF-L) mRNA triggers aggregation of NF-L and mutant superoxide dismutase 1 proteins in neuronal cells.

The pathogenesis of neurodegenerative diseases is believed to involve abnormal aggregation of proteins, but the mechanisms initiating protein aggregation are unclear. Here we report a novel phenomenon that could be instrumental in triggering protein aggregation in neurodegenerative diseases. We show that the 3' untranslated region (3'UTR) of a light neurofilament (NF-L) transcript enhances the reactivity of its own translated product and leads to loss of solubility and aggregation of NF-L protein and to coaggregation of mutant superoxide dismutase 1 (SOD1) protein. Full-length mouse NF-L cDNAs, with and without NF-L 3'UTR, were fused to the C terminus of a green fluorescent protein (GFP) reporter gene, and the GFP-tagged NF-L proteins were examined in transfected Neuro2a cells. The GFP-tagged NF-L protein expressed from the transgene containing NF-L 3'UTR, but not from the transgene lacking NF-L 3'UTR, colocalizes with endogenous heavy neurofilament protein and, at high-level expression, leads to loss of solubility and aggregation of GFP-tagged NF-L protein. Aggregation of GFP-tagged NF-L protein triggers coaggregation and loss of solubility of coexpressed DsRed-tagged mutant (G93A) SOD1 protein but not wild-type SOD1 protein. Deletional mutagenesis maps the RNA sequence causing aggregation of GFP-tagged NF-L protein to the proximal 45 nucleotides of NF-L 3'UTR. This is the site of a major destabilizing element in NF-L RNA and binding site for RNA-binding proteins. Our findings support a working model whereby NF-L RNA, or cognate RNA-binding factors, enhances the reactivity of NF-L protein and provides a triggering mechanism leading to aggregation of NF-L and other proteins in neurodegenerative diseases.

3' Untranslated Regions↗

PubMed2004

Polarographic determination of diazepam with its parallel catalytic wave in the presence of persulfate.

A new method for the determination of diazepam was proposed based on its polarographic catalytic wave in the presence of persulfate. In 0.20 M NaAc-HAc (pH 4.7)-1.0 x 10(-2) M K(2)S(2)O(8) supporting electrolyte, the reduction wave of diazepam with peak potential -0.89 V (versus SCE) was catalyzed, producing a parallel catalytic wave. The peak current of the catalytic wave was 15 times higher than that of the corresponding reduction wave for 4.0 x 10(-6) M diazepam, and was rectilinear to diazepam concentration in the range of 5.6 x 10(-8) to 8.9 x 10(-6) and 8.8 x 10(-6) to 2.0 x 10(-4) M. The detection limit was 9.6 x 10(-9) M. The mechanism of the parallel catalytic wave of diazepam was discussed.

Buffers↗

PubMed2004

Fertilization of IVF/ICSI using sibling oocytes from couples with subfertile male or unexplained infertility.

The significance of the performance of conventional in vitro fertilization and intracytoplasmic sperm injection (IVF/ICSI) using sibling oocytes from couples with subfertile male or unexplained infertility was evaluated. A total of 410 sibling oocyte cumulus-corona complexes (OCCC) from 21 couples with subfertile male (group A) and 11 unexplained infertile couples (group B) were randomly divided, in order of retrieval, into two groups inseminated either by conventional IVF or by ICSI. The treatment outcomes and the influence of infertility factors on fertilization in each group were compared. The results showed that although the two pronuclear (2PN) fertilization rate per injected sibling oocytes was significantly higher after ICSI (group A: 68.2% +/- 28.8%; group B: 66.2% +/- 24.9%) than after conventional IVF (group A: 41.8% +/- 32.7%; group B: 40.1% +/- 22.1%), the other variables studied included: the fertilization rates of per allocated sibling oocytes IVF/ICSI, the fertilization rates of sibling oocytes IVF/ICSI after excluding failed IVF fertilization cycles, as well as the cleavage rates of normal fertilization were not statistically significant (P>0.05). Similarly, though the total fertilization failure rate in the IVF group (group A: 42.9%; group B: 36.4%) was significantly higher than in the ICSI group (group A: 4.8%; group B: 0), we did not cancel cycles due to the normal fertilization of sibling oocytes. Embryo transfer was possible in all 32 couples. There were 10 clinical pregnancies in the two groups. We also discovered a possible association between some semen parameters and sperm functions of group A, and women age and duration of infertility of group B and fertilization. It is suggested that adoption of the split IVF/ICSI technology in the above cases may help eliminate fertilization failures. This is also a useful method to investigate the effect of single factor on the employment of assisted reproductive technology.

Embryo Transfer↗