Biomedical subjects

Qing Chang

Publications and source records attributed to Qing Chang.

At least 55 records · Page 3Linked to original sources

PubMed2005

[Hypothesis on generating and tracer gas study regarding transmission of severe acute respiratory syndrome through ventilation system in a general hospital].

OBJECTIVE: By measuring airflow and ventilation distribution of ward building, to explore and verify the hypothesis of airborne transmission and risk factor of severe acute respiratory syndrome (SARS) nosocomial infection. METHODS: Tracer gas (perfume of plant oil) was emitted to the bathroom of wards when SARS index patient lived. Six different experimental situations were designed to control the status of exhaust fan in bathrooms, exhaust fan in the top of building and fresh air exchange system. The concentration of perfume was separately measured by 4 groups of lab workers and recorded blindly by the scores of "tenth degree". RESULTS: Tracer gas was detected from the wards of 8th to 13th floor. CONCLUSION: Architecture and ventilation system of the inpatient building in the hospital contributed to the aerodynamic condition of SARS nosocomial infection through airborne transmission. The distribution of tracer gas in the wards was associated with SARS patients in this building. It was possible that SARS could have been transmitted to for distance by aerosol or other carriers.

Air Microbiology↗

PubMed2005

[Effects of varying the opaque thickness and the type of metal ceramic alloy on color].

OBJECTIVE: To compare the color differences of different metal bases and different opaque thickness, and evaluate the best thickness of opaque on different metal bases. METHODS: Precious metal, gold sediment and Ni-Cr plates were prepared as bases, then opaque samples of 0.05, 0.1, 0.2, 0.3, 0.4 and 0.5 mm thickness were fabricated on such plates. Minolta chromatics meter CR-321 was used to examine the color properties of these samples, and deltaE was calculated to evaluate the color difference of the specimens. RESULTS: For the restoration based on Ni-Cr and precious alloys, the color of restorations was not affected by the color of metal bases as the thickness of opaque reached 0.3 mm, and the chromatic value deltaE < 1.5 NBS. For the restoration based on gold sediment, the color of restoration was not affected by the color of metal as the thickness of opaque reached 0.1 mm, and the chromatic value deltaE < 1.5 NBS. CONCLUSION: Different opaque thickness was necessary to obtain ideal color appearance in clinic. As the opaque thickness increased, the color of restoration based on Ni-Cr and noble metal increased but the color of restoration based on gold sediment decreased.

Color↗

PubMed2004

Molecular determinants in TRPV5 channel assembly.

The epithelial Ca(2+) channels TRPV5 and TRPV6 mediate the Ca(2+) influx in 1,25-dihydroxyvitamin D(3)-responsive epithelia and are therefore essential in the maintenance of the body Ca(2+) balance. These Ca(2+) channels assemble in (hetero)tetrameric channel complexes with different functional characteristics regarding Ca(2+)-dependent inactivation, ion selectivity, and pharmacological block. Glutathione S-transferase pull-downs and co-immunoprecipitations demonstrated an essential role of the intracellular N- and C-tails in TRPV5 channel assembly by physical interactions between N-N tails, C-C tails, and N-C-tails. Patch clamp analysis in human embryonic kidney (HEK293) cells and (45)Ca(2+) uptake experiments in Xenopus laevis oocytes co-expressing TRPV5 wild-type and truncated proteins indicated that TRPV5 Delta N (deleted N-tail) and TRPV5 Delta C (deleted C-tail) decreased channel activity of wild-type TRPV5 in a dominant-negative manner, whereas TRPV5 Delta N Delta C (deleted N-tail/C-tail) did not affect TRPV5 activity. Oocytes co-expressing wild-type TRPV5 and TRPV5 Delta N or TRPV5 Delta C showed virtually no wild-type TRPV5 expression on the plasma membrane, whereas co-expression of wild-type TRPV5 and TRPV5 Delta N Delta C displayed normal channel surface expression. This indicates that TRPV5 trafficking toward the plasma membrane was disturbed by assembly with TRPV5 Delta N or TRPV5 Delta C but not with TRPV5 Delta N Delta C. TRPV5 channel assembly signals were refined between amino acid positions 64-77 and 596-601 in the N-tail and C-tail, respectively. Pull-down assays and co-immunoprecipitations demonstrated that N- or C-tail mutants lacking these critical assembly domains were unable to interact with tails of TRPV5. In conclusion, two domains in the N-tail (residues 64-77) and C-tail (residues 596-601) of TRPV5 are important for channel subunit assembly, subsequent trafficking of the TRPV5 channel complex to the plasma membrane, and channel activity.

Amino Acid Sequence↗

PubMed2004

Expression of TREM-1 mRNA in acute pancreatitis.

AIM: To explore the expression of triggering receptor expressed on myeloid cells (TREM-1) mRNA in acute pancreatitis (AP). METHODS: Using the reverse transcription polymerase chain reaction (RT-PCR), we examined the expression of TREM-1 mRNA in 10 cases of mild acute pancreatitis (MAP), 8 cases of severe acute pancreatitis (SAP), and 10 cases of healthy control subjects. And we also examined the expression of TREM-1 mRNA in 14 cases of AP (including 10 MAP and 4 SAP) before treatment, after successful therapy and clinically cured. RESULTS: The expression of TREM-1 mRNA in the groups of MAP, SAP patients and healthy control subjects was 0.771+/-0.274, 1.092+/-0.331 and 0.459+/-0.175, respectively; there was a significant difference among the three groups (P<0.05). And there was also a significant difference between the AP patients (0.914+/-0.341) and healthy control subjects (0.459+/-0.175) (P<0.05). Moreover, in the 14 cases of AP, before treatment, after successful therapy and clinically cured, the expression of TREM-1 mRNA was 0.905+/-0.226, 0.739+/-0.169 and 0.633+/-0.140, respectively, and there was a significant difference among the three stages (P<0.05). CONCLUSION: The expression of TREM-1 mRNA in the patients with AP increases obviously, and correlates with the degree of AP. Furthermore, the expression of TREM-1 mRNA is distinctly different at the different stages of AP. It indicates TREM-1 may play an important role in the occurrence and development of AP.

Acute Disease↗

PubMed2004

Inhibition of potassium currents in outer hair cells and Deiters' cells from guinea pig cochlea by linopirdine.

To study the functional expression of KCNQ gene in outer hair cells (OHCs) and Deiters' cells, the effects of linopirdine on the whole cell K(+) current were investigated by using the whole cell variant of patch clamp technique in the present study. The outward tetraethylammonium (TEA)-sensitive K(+) current and the inward K(+) current (I(Kn)) in OHCs were recorded and measured before and after the administration of linopirdine. Simultaneously, the whole cell currents in Deiters?cells were also observed in normal solution and in the presence of linopirdine. After the application of 100 micromol/L linopirdine to OHCs, the peak K(+) current was reversibly blocked and the late K(+) current was partly reduced. In addition, the decay time constant of the TEA-sensitive K(+) current was prolonged in the presence of 100 micromol/L linopirdine. The inward current in OHCs was totally inhibited after the superfusion of 100 mmol/L and 200 micromol/L linopirdine respectively. The outward rectifier K(+) current (Ik) was the dominant K(+) current in the whole cell currents in Deiters' cells. In the presence of 200 micromol/L linopirdine, the I(K) current was not significantly affected. Our findings demonstrate that the KCNQ heteromeric or homomeric potassium channel is possibly the molecular basis for the peak outward K(+) current and that the inward I(Kn) current is mediated by KCNQ potassium channel. KCNQ potassium channel in OHCs can not only permit the K(+) efflux but also limit the depolarization. In the present study, no expression of KCNQ potassium channel is found in Deiters' cells.

Animals↗

PubMed2004

Effect of octreotide on human pancreatic cancer cells after transfected with somatostatin receptor type 2 gene.

AIM: To observe the effect of octreotide on apoptosis rate of human pancreatic cancer cells PC-3 after transfected with somatostatin receptor type 2 (SST2) gene. METHODS: SST2 plasmid was transfected into PC-3 cells by liposome. Result of transfection was detected by immunocytochemical staining and Western blotting. Apoptosis rates of PC-3 cells under different dosages of octreotide were measured by MTT assay and flow cytometry (FCM). RESULTS: Apoptosis rate caused by octreotide of transfected PC-3 cells was 7.56+/-1.06% at the dosage of 0.20 microg/mL, 9.25+/-1.73% at the dosage of 0.40 microg/mL and 14.18+/-2.71% at the dosage of 0.80 microg/mL. Apoptosis rate caused by octreotide of non-transfected PC-3 cells was 5.76+/-0.75% at the dosage of 0.20 microg/mL, 6.69+/-0.80% at the dosage of 0.40 microg/mL and 7.26+/-1.28% at the dosage of 0.80 microg/mL. Transfected PC-3 cells growth inhibition rate caused by octreotide was 9.36+/-1.34% at the dosage of 0.20 microg/mL, 12.03+/-1.44% at the dosage of 0.40 microg/mL and 20.23+/-4.21% at the dosage of 0.80 microg/mL. Non-transfected PC-3 cells growth inhibition rate caused by octreotide was 6.44+/-0.66% at the dosage of 0.20 microg/mL, 7.65+/-0.88% at the dosage of 0.40 microg/mL and 9.29+/-1.32% at the dosage of 0.80 microg/mL. We found that octreotide caused higher apoptosis rate and inhibition rate in transfected groups than in non-transfected groups (P<0.05) at the tested dosages (0.20, 0.40 and 0.80 microg/mL). CONCLUSION: Deficiency of SST2 was probably the major reason why octreotide had little effect on PC-3 cells. Transfecting SST2 gene could strengthen the ability of octreotide of killing PC-3 cells. It provided an experimental evidence for using both octreotide and transfection with SST2 gene on clinical treatment of pancreatic cancer.

Apoptosis↗

PubMed2004

Inhibition of HIV-1 replication by GB virus C infection through increases in RANTES, MIP-1alpha, MIP-1beta, and SDF-1.

Background People coinfected with HIV and GB virus C (GBV-C) have lower mortality than HIV-positive individuals without GBV-C infection. HIV uses either of the chemokine receptors CCR5 and CXCR4 for entry into CD4-positive cells. Longer survival in HIV-positive individuals is associated with high serum concentrations of ligands for CCR5 (RANTES [regulated on activation, normal T-cell expressed and secreted] and macrophage inflammatory proteins [MIP] 1alpha and 1beta) and CXCR4 (stromal-derived factor [SDF-1]), and with decreased expression of CCR5 on lymphocytes. Methods Peripheral-blood mononuclear cells were coinfected with GBV-C and HIV, and HIV replication was monitored by measuring infectivity and HIV p24 antigen production. Chemokine secretion was measured by ELISA, chemokine-receptor expression by flow cytometry, and cellular chemokine mRNA expression by differential hybridisation. Findings GBV-C infection of peripheral-blood mononuclear cells resulted in decreased replication of both clinical and laboratory HIV strains that use either CCR5 or CXCR4 as their coreceptor. Inhibition was related to the dose and timing of the GBV-C infection. Expression of mRNA for RANTES, MIP-1alpha, MIP-1beta, and SDF-1 and secretion of the chemokines into culture supernatants were higher in GBV-C-infected cells than in mock-infected cells. The inhibitory effect of GBV-C on HIV replication was blocked by incubation with neutralising antibodies against the relevant chemokines, and surface expression of CCR5 was significantly lower in GBV-C-infected cells than in mock-infected cells. Interpretation GBV-C induces HIV-inhibitory chemokines and reduces expression of the HIV coreceptor CCR5 in vitro. This study provides insight into the epidemiological association between GBV-C infection and longer survival in HIV-infected individuals.

Cells, Cultured↗

PubMed2004

Molecular analysis of PinX1 in medulloblastomas.

Our group has previously demonstrated a high frequency of allelic loss on the short arm of chromosome 8 and identified a region of homozygous deletion of 1.41 Mb, flanked by D8S520 and D8S1130, on 8p23.1 in medulloblastomas, suggesting the presence of a tumor suppressor gene in this critical deletion region. The aim of our study was to investigate whether PinX1, a newly identified gene whose product is a potent inhibitor of telomerase, is the target gene in the homozygous deletion region identified in medulloblastomas. We assessed for alterations in gene sequence and transcript expression of PinX1, as well as the correlation between PinX1 expression and telomerase activity in a series of 52 medulloblastomas, 3 medulloblastoma cell lines (D283, D341 and Daoy) and 4 primitive neuroectodermal tumors (PNETs). Direct sequence analysis of all 7 exons and splice junctions of the PinX1 gene revealed no somatic mutations but 11 genetic polymorphisms. Transcript expression of PinX1, as evaluated by reverse transcription-polymerase chain reaction, in microdissected tumors and normal cerebellum showed 2 transcript variants, corresponding to the full-length form and an alternative spliced variant lacking exon 6, in all samples. This result indicated that PinX1 expression was not suppressed in medulloblastomas. Using the telomeric repeat amplification protocol (TRAP) assay, 13 of 19 (68%) medulloblastomas, 1 of 2 PNETs and all 3 cell lines showed telomerase activity. There is no significant correlation between PinX1 transcript expression and telomerase activity, but our results showed that telomerase activation is involved in medulloblastomas. Taken together, our results suggest that PinX1 does not play a major role in the oncogenesis of medulloblastomas.

Adolescent↗

PubMed2004

Antiangiogenic effect of somatostatin receptor subtype 2 on pancreatic cancer cell line: Inhibition of vascular endothelial growth factor and matrix metalloproteinase-2 expression in vitro.

AIM: To investigate the anti-angiogenic effect of somatostatin receptor subtype 2 (SSTR2) gene transfer into pancreatic cancer cell line PC-3, and the mechanisms involved in this effect. METHODS: The full length human SSTR2 cDNA was introduced into pancreatic cancer cell line PC-3 by lipofectamine-mediated transfection. Positive clones were screened by G418 and stable expression of SSTR2 was detected by immunohistochemistry SABC methods and RT-PCR. Enzyme-linked immunosorbent assay (ELISA) was used to detect vascular endothelial growth factor (VEGF) levels in the cell culture supernatants of SSTR2-expressing cells, vector control and mock control cells. Furthermore, the expressions of VEGF and matrix metalloproteinase-2 (MMP-2) were detected by immunohistochemistry SABC methods and RT-PCR in these cells. RESULTS: VEGF levels in the cell culture supernatants were significantly reduced in the SSTR2-expressing cells (first week, 172.63+/-21.2 ng/L and after two months, 198.85+/-26.44 ng/L) compared with the vector control (first week, 790.39+/-86.52 ng/L and after two months, 795.69+/-72.35 ng/L) and mock control (first week, 786.42+/-90.62 ng/L and after two months, 805.32+/-84.36 ng/L) (P<0.05). The immunohistochemical assay showed a significant reduction of the integral optical density of VEGF and MMP-2 in the SSTR2-expressing cells (42.25+/-8.6 and 70.5+/-6.25, respectively) compared with the vector control (85.75+/-12.9 and 110.52+/-13.5, respectively) and mock control (82.6+/-9.28 and 113.56+/-9.62, respectively) (P<0.05). Conversely, the average gray value of VEGF and MMP-2 was significantly increased in the SSTR2-expressing cells (121.56+/-8.43 and 134.46+/-19.95, respectively) compared with the vector control (55.72+/-5.6 and 62.26+/-12.68, respectively) and mock control cells (58.48+/-6.2 and 65.49+/-9.16, respectively) (P<0.05). Moreover, the expressions of VEGF mRNA and MMP-2 mRNA were significantly reduced in the SSTR2-expressing cells (0.1384+/-0.017 and 0.2343+/-0.070, respectively) compared with the vector control (1.024+/-0.117 and 0.806+/-0.119, respectively) and mock control (1.085+/-0.105 and 0.714+/-0.079, respectively) (P<0.05). CONCLUSION: The expression of reintroduced human SSTR2 gene exerts its antiangiogenic effects by down-regulating the expressions of the factors involved in tumor angiogenesis and metastasis, suggesting SSTR2 gene transfer as a new strategy of gene therapy for pancreatic cancer.

Cell Line, Tumor↗

PubMed2004

Survivin expression induced by doxorubicin in cholangiocarcinoma.

AIM: To study the role of survivin expression induced by chemotherapy agent (doxorubicin) in the development and anti-chemotherapy of cholangiocarcinoma. METHODS: Expression of survivin was detected by SP immunohistochemical technique in 33 cases of cholangiocarcinoma, 28 cases of adjacent noncancerous bile duct, and 5 cases of benign bile duct lesions. Low concentration of doxorubicin (0.05 mg/l) was added in cultured cholangiocarcinoma cell line (QBC939). The expression of survivin was detected by RT-PCR and Western blot at 24 h and 48 h after adding doxorubicin. RESULTS: Survivin was expressed in 24 of 33 cholangiocarcinoma cases (72.7%). In contrast, no expression of survivin in adjacent noncancerous and benign bile duct lesions was observed (P<0.01). No correlation was found between survivin expression and clinical features. Doxorubicin could markedly (P<0.001) up-regulate survivin mRNA and protein expression of QBC939 cells. CONCLUSION: Overexpression of survivin in cholangiocarcinomas may play an important role in the development of cholangiocarcinoma, its relationship with prognosis of cholangiocarcinoma deserves further investigation. Higher expression of survivin is induced by doxorubicin in QBC939. Survivin expression may resist apoptosis induced by chemotherapy agents.

Adult↗

PubMed2004

Impaired and spared cholinergic functions in the hippocampus after lesions of the medial septum/vertical limb of the diagonal band with 192 IgG-saporin.

To lesion the cholinergic input to the hippocampus, rats received injections of 192 IgG-saporin into the medial septum/vertical limb of the diagonal band (MS/VDB). The lesions produced near-total loss of choline acetyltransferase (ChAT)-positive neurons in the MS/VDB. The loss was accompanied, however, by only partial decreases (to 40% of control levels) in acetylcholine (ACh) release in the hippocampus. Moreover, ACh release in the hippocampus increased when lesioned and control rats were tested on a spontaneous alternation task, indicating that there was significant residual cholinergic function in the hippocampus. The lesions were sufficient to impair spontaneous alternation scores. However, this impairment could be reversed by either systemic or intra-hippocampal injections of the indirect cholinergic agonist, physostigmine, providing additional evidence of residual and effective cholinergic functions in the hippocampus of lesioned rats. Moreover, systemic injections of physostigmine at doses that produced mild tremors in control rats led to more severe tremors in the lesioned rats, suggesting upregulation of cholinergic mechanisms after saporin lesions, likely in brain areas other than the hippocampus. Thus, these findings provide evidence for decreases in cholinergic input to the hippocampus accompanied by deficits on a spontaneous alternation tasks. The findings also provide evidence for considerable residual cholinergic input to the hippocampus after saporin lesions of the MS/VDB. Together, the results suggest that 192 IgG-saporin lesions of the MS/VDB, using methods often employed, do not fully remove septohippocampal cholinergic input to the hippocampus but are nonetheless sufficient to produce impairments on a task impaired by hippocampal lesions.

Acetylcholine↗

PubMed2004

The expression of VIP and SP in the cochlea of spontaneously hypertensive rats and its implication.

To investigate the expression of vasoactive intestinal peptide (VIP) and substance P (SP) in the cochlea of spontaneously hypertensive rat (SHR), and to assess the function of VIP and SP in the cochlea following the damage of hypertension, hearing thresholds of ABR were observed and the fixative (4% paraformaldehyde) was pumped through the circulatory system. Adult Wistar rats (3 months, n=20) served as the control group and SHRs (3 months, n=20) as the hypertension group. Bullas were taken out and cochleas were irrigated in vitro with the same fixative. The number of base turn's spiral ganglions in the sections was counted. The expression of VIP and SP were detected by SABC method and the images of the sections were analyzed. The number of base turn's spiral ganglsons in the hypertension group was significantly less than in the normal group (P<0.01). VIP and SP were expressed in the spiral ganglion cytoplasma and stria vascularis of the two groups. There were no significant difference in the expression of VIP and SP in spiral ganglion cytoplasma (P>0.05) between the two groups. However, in stria vascularis the expression of VIP in the hypertension group was higher than in the normal group (P<0.05), and no significant difference in SP was found between the two groups. It was suggested that VIP not only contributed to the regulation of the cochlea microcirculation, but also made the neurotransmitter in the pathway of the auditory system. However, SP made only the neurotransmitter in the pathway of the auditory system.

Animals↗

PubMed2004

Detection of left ventricular regional relaxation abnormalities in patients with hypertrophic cardiomyopathy by quantitative tissue velocity imaging.

To assess the left ventricular regional relaxation abnormalities in patients with hypertrophic cardiomyopathy (HCM) by quantitative tissue velocity imaging (QTVI), Doppler echocardiography and QTVI were performed in HCM (n=10) and healthy subjects (n=11) at apical long-axis, two-chamber and four-chamber views. Regional early diastolic velocity (rVe) and regional atrial contraction (rVa) were measured at each segment of ventricular middle, basal and annular levels. Mean rVe and mean rVa at three levels as well as mean rVe/rVa ratio were calculated. Our results showed that transmitral inflow peak velocities during early diastole (E) and atrial contraction (A) were also measured and E/A ratio was calculated. The rVe of all left ventricular segments in HCM were lower than those in healthy subjects (P<0.05), but compared with healthy subjects majority of rVa in HCM were not different except inferior wall and anterior wall. E between HCM and healthy subjects was different (P=0.036), while mean rVe between them was significantly different (P<0.0001). Mean rVa and mean rVe/rVa of three levels were lower in HCM than in healthy subjects (P<0.05), but there were no differences in A and E/A between them (P=0.22, P=0.101). Left ventricular regional myocardial relaxation is reduced in HCM. Transmitral inflow E and A are influenced by preload, relaxation of myocardium and atrial contraction, etc., while rVe and rVa reflect myocardial relaxation function independently. QTVI is more sensitive and more accurate than conventional Doppler imaging for characterizingregional diastolic properties in HCM.

Adolescent↗

PubMed2004

Nitric oxide formation contributes to beta-adrenergic dilation of epicardial coronary arteries in response to intravenous administration of dobutamine in dogs.

To examine the role of nitric oxide in the beta-adrenergic vasodilation of epicardial coronary arteries in dogs, 12 dogs were instrumented for measurement of left anterior descending coronary artery diameter by transthoracic echocardiography before and after dobutamine (5 microg/kg/min IV) with and without intracoronary infusion of NG-monomethyl-L-arginine (L-NMMA) (1 mg/kg). In all 12 dogs, the diameter of left anterior descending coronary artery increased significantly from 2.35 +/- 0.25 mm to 2.59 +/- 0.24 mm (P<0.001) after dobutamine administration. In 6 of the 12 dogs, the percent change in left anterior descending coronary artery diameter induced by dobutamine decreased significantly from 12.5% +/- 8.6% to -1.5% +/- 5.4% (P<0.05) after the administration of intracoronary L-NMMA (1 mg/kg for 5 min) to block nitric oxide synthesis from L-arginine. The study demonstrated that nitric oxide formation contributes to the beta-adrenergic dilatory response of epicardial coronary arteries to dobutamine in dogs.

Adrenergic beta-Agonists↗

PubMed2004

VH3 gene expression in children with HIV infection.

OBJECTIVE: To study immunoglobulin heavy chain variable region (V(H)) gene expression in HIV-uninfected (HIV-) and HIV-infected (HIV+) children. METHODS: A retrospective, observational study was performed by PCR-ELISA to examine IgM and IgG V(H) gene family expression among peripheral CD19-positive B cells. The subjects were 10 HIV+ children with, and 11 HIV+ children without a history of invasive pneumococcal disease (IPD) and 12 HIV- children. The ages of the HIV+ and HIV- children, and the CD4 lymphocyte counts and viral loads (VL) of the HIV+ /IPD- and HIV+ /IPD- children were statistically similar. Rearranged V(H)3 gene libraries were constructed from 3 HIV+ /IPD- children to examine individual gene expression. RESULTS: The proportion of IgG V(H)3 expression among HIV+ /IPD- was lower than that of HIV- children, but the proportion of IgG V(H)3 expression among HIV+ /IPD+ children was not significantly different from that of HIV- children. IgG V(H)3 expression was positively, whereas IgM V(H)3 expression was inversely correlated with the VL among HIV+ /IPD+, but not HIV+ /IPD- children. IgM V(H) gene family expression did not differ between HIV+ and HIV- children. CONCLUSION: HIV+ children manifest qualitative and quantitative differences in V(H)3 expression, which may be influenced by IPD.

Bacteremia↗

PubMed2004

Inactivation of dorsolateral striatum impairs acquisition of response learning in cue-deficient, but not cue-available, conditions.

Rats received bilateral injections of lidocaine or artificial cerebrospinal fluid (aCSF) into the doisolateral striatum 6 min prior to training in either a plus- or T-shaped maze under cue-poor or cue-available conditions. Lidocaine injections significantly impaired acquisition in the cue-poor environments, but not in the cue-available environments. In addition, aCSF control rats trained in a plus-maze in a cue-poor environment reached criterion much more rapidly than did rats trained in a cue-available environment. These findings suggest that cue availability can permit acquisition of response learning in a manner that is not dependent on activity of the striatum. However, in a cue-poor environment, alternate strategies may be less readily available, revealing more efficient striatal involvement in response learning.

Anesthetics, Local↗

PubMed2004

Protective and nonprotective human immunoglobulin M monoclonal antibodies to Cryptococcus neoformans glucuronoxylomannan manifest different specificities and gene use profiles.

The features of protective murine antibodies to the Cryptococcus neoformans capsular polysaccharide glucuronoxylomannan (GXM) have been rigorously investigated; however, the characteristics of protective human antibodies to GXM have not been defined. We produced monoclonal antibodies (MAbs) from XenoMouse mice (transgenic mice that express human immunoglobulin M [IgM], IgG2, and kappa) which were immunized with a C. neoformans serotype D strain 24067 GXM-diphtheria toxoid conjugate. This study reports the specificity and efficacy of three human IgM MAbs, G14, G15, and G19, generated from these mice. Each MAb was specific for GXM, but G14 and G19 had different specificity based on their binding to serotype A strain H99 and SB4 GXMs, to which G15 did not bind. Nucleic acid sequence analysis revealed that G15 uses V(H)3-64 in the germ line configuration. G14 and G19 use V(H)6-1, which has somatic mutations. All of the MAbs use V kappa DPK22/A27. Studies of MAb efficacy in BALB/c mice showed that administration of 0.1 mg, but not 1 or 0.01 mg, of G15 prolonged survival against lethal C. neoformans strain 24067 challenge, whereas G14 and G19 were not protective at any dose. This panel of MAbs illustrates that serotype D GXM has epitopes that elicit human antibodies that can be either protective or nonprotective. Our findings suggest that V(H) gene use may influence GXM specificity and efficacy, and they provide insights into the possible contribution that V(H) gene use may have in resistance and susceptibility to cryptococcosis.

Amino Acid Sequence↗

PubMed2004

Alteration of somatostatin receptor subtype 2 gene expression in pancreatic tumor angiogenesis.

AIM: To explore the difference of somatostatin receptor subtype 2 (SST2R) gene expression in pancreatic cancerous tissue and its adjacent tissue, and the relationship between the change of SST2R gene expression and pancreatic tumor angiogenesis related genes. METHODS: The expressions of SST2R, DPC4, p53 and ras genes in cancer tissues of 40 patients with primary pancreatic cancer, and the expression of SST2R gene in its adjacent tissue were determined by immunohistochemiscal LSAB method and EnVision(TM) method. Chi-square test was used to analyze the difference in expression of SST2R in pancreatic cancer tissue and its adjacent tissue, and the correlation of SST2R gene expression with the expression of p53, ras and DPC4 genes. RESULTS: Of the tissue specimens from 40 patients with primary pancreatic cancer, 35 (87.5%) cancer tissues showed a negative expression of SST2R gene, whereas 34 (85%) a positive expression of SST2R gene in its adjacent tissues. Five (12.5%) cancer tissues and its adjacent tissues simultaneously expressed SST2R. The expression of SST2R gene was markedly higher in pancreatic tissues adjacent to cancer than in pancreatic cancer tissues (P<0.05). The expression rates of p53, ras and DPC4 genes were 50%, 60% and 72.5%, respectively. There was a significant negative correlation of SST2R with p53 and ras genes (chi(1)(2)=9.33, chi(2)(2)=15.43, P<0.01), but no significant correlation with DPC4 gene (chi(2)=2.08, P>0.05). CONCLUSION: There was a significant difference of SST2R gene expression in pancreatic cancer tissues and its adjacent tissues, which might be one cause for the different therapeutic effects of somatostatin and its analogs on pancreatic cancer patients. There were abnormal expressions of SST2R, DPC4, p53 and ras genes in pancreatic carcinogenesis, and moreover, the loss or decrease of SST2R gene expression was significantly negatively correlated with the overexpression of tumor angiogenesis correlated p53 and ras genes, suggesting that SST2R gene together with p53 and ras genes may participate in pancreatic cancerous angiogenesis.

Adenocarcinoma↗