Biomedical subjects

G Yang

Publications and source records attributed to G Yang.

At least 199 records · Page 11Linked to original sources

PubMed1999

cDNA cloning and expression of acutin.

Acutin, a thrombin-like enzyme was purified from Agkistrodon acutus venom in three steps by DEAE-Sepharose CL-6B, Superose 12 column on FPLC and Mono-Q column chromatographies. Its first 15 N-terminal amino acid residues sequence was then determined and the acutin cDNA was isolated from venom gland total RNA using RT-PCR. Determination of its nucleotide sequence allowed elucidation of the amino acid sequence of mature peptide for the first time. The mature acutin has 233 amino acids and its amino acid sequence exhibits significant homology with those of thrombin-like enzymes from crotaline snakes venoms. Based on the homology, the catalytic residues and disulfide bridges of acutin were deduced to be as follows: catalytic residues, His41, Asp84 and Ser179; and disulfide bridges, Cys7-Cys139, Cys26-Cys42, Cys74-Cys231, Cys118-Cys185, Cys150-Cys164, Cys175-Cys200. The recombinant acutin has been expressed in E. coli and purified by affinity column. The renatured recombinant acutin is reported for the first time to have the activity of clotting fibrinogen and arginine-esterase.

Agkistrodon↗

PubMed1999

The angiotensinogen gene is expressed in both astrocytes and neurons in murine central nervous system.

Two transgenic mouse models were used to examine the cellular localization of angiotensinogen (AGT) in the brain. The first model was previously described in detail and consists of a human AGT genomic transgene containing all exons and introns of the gene and 1. 2 kb of the 5' flanking DNA. The second model contains a fusion between 1.2 kb of HAGT 5' flanking DNA and the beta-gal reporter gene which exhibits a similar pattern of tissue-specific expression to the HAGT transgene. Expression of both transgenes qualitatively mirrors the expression of endogenous AGT. Double staining of transgenic mouse brain sections with X-gal and GFAP revealed that a majority of beta-gal activity was localized to astrocytes in almost all brain areas. However, both beta-gal activity as identified by X-gal, and HAGT mRNA as detected by in situ hybridization, were also found in neurons in restricted areas of the brain, including the mesencephalic trigeminal nucleus (meV), subfornical organ (SFO) and the external lateral parabrachial nucleus (elPB). The expression of these transgenes provides the first convincing evidence for AGT gene expression in neurons in the brain. We further report by angiotensin II (Ang-II) immunostaining in rat brains after selective lesioning, that Ang-II is likely involved in a neuronal pathway from the PB to the amygdala (Ce). Finally, we performed double-labeling, first by retrograde labeling of HRP injected into the Ce, and then by X-gal on PB neurons in beta-gal transgenic mice, and identified doubly labeled neurons. Based on these results, we propose that AGT is generated in neurons in the elPB, transported to the Ce and converted into Ang-II locally to exert is biological functions.

Angiotensinogen↗

PubMed1999

Micellar electrokinetic capillary chromatography of psoralen and isopsoralen.

In this paper, a micellar electrokinetic capillary chromatography (MEKC) method to analyze the active components of psoralen and isopsoralen in the Chinese herb Psoralea corylifolia L. was developed. It was found that the optimum separation condition for the analysis of these compounds was a buffer solution which contained phosphate, borate and sodium dodecyl sulfate (pH 9.2). Through optimization of the experimental condition, the two isomers could be baseline-separated and their contents in the methanol-extracted sample were quantitatively analyzed.

Buffers↗

PubMed1999

Effects of L-tetrahydropalmatine on energy metabolism, endothelin-1 and NO during acute cerebral ischemia-reperfusion of rats.

To investigate the effects of L-tetrahydropalmatine (L-THP) on energy metabolism, endothelin-1 (ET-1) and NO during acute cerebral ischemia-reperfusion of rats, 24 Wistar rats were randomly divided into four groups, with 6 rats in each group: sham-operation group, simple ischemia group, ischemia-reperfusion group and treatment group (L-THP group). Cerebral ATP, lactate, ET-1 and NO levels were measured in all groups. Our results showed that treatment with L-THP could increase cerebral ATP levels, but decrease cerebral lactate, ET-1 and NO concentrations during ischemia-reperfusion in the treatment group. It is concluded that L-THP could improve cerebral energy metabolism and protect the injured brain tissue, the mechanism of which might be related to suppression of overproduction of ET-1 and NO.

Animals↗

PubMed1999

Perioperative cimetidine application modulates natural killer cells in patients with colorectal cancer: a randomized clinical study.

Thirty-eight colorectal cancer patients were randomly assigned to treatment group, which took cimetidine in the perioperative period, and control group to which no drug was given. Twenty healthy volunteers served as normal controls. NK cells were measured by immunocytochemical technique. The results showed that NK percentages before treatment in both groups of patients were significantly lower than those in normal controls (P < 0.05). NK cell percentages at admission, before operation, on the 2nd and the 10th postoperative days were 14.84 +/- 4.41, 15.74 +/- 3.75, 17.21 +/- 3.69, 21.05 +/- 4.54, respectively, for the treatment group, and 15.00 +/- 2.77, 13.05 +/- 2.46, 14.21 +/- 2.19, 15.58 +/- 1.68, respectively, for control group. The difference was statistically significant (P < 0.01), suggesting that the perioperative administration of cimetidine could help restore NK cells in colorectal cancer patients.

Cimetidine↗

PubMed1999

Direct observation of one-dimensional diffusion and transcription by Escherichia coli RNA polymerase.

The dynamics of nonspecific and specific Escherichia coli RNA polymerase (RNAP)-DNA complexes have been directly observed using scanning force microscopy operating in buffer. To this end, imaging conditions had to be found in which DNA molecules were adsorbed onto mica strongly enough to be imaged, but loosely enough to be able to diffuse on the surface. In sequential images of nonspecific complexes, RNAP was seen to slide along DNA, performing a one-dimensional random walk. Heparin, a substance known to disrupt nonspecific RNAP-DNA interactions, prevented sliding. These observations suggest that diffusion of RNAP along DNA constitutes a mechanism for accelerated promoter location. Sequential images of single, transcribing RNAP molecules were also investigated. Upon addition of 5 microM nucleoside triphosphates to stalled elongation complexes in the liquid chamber, RNAP molecules were seen to processively thread their template at rates of 1.5 nucleotide/s in a direction consistent with the promoter orientation. Transcription assays, performed with radiolabeled, mica-bound transcription complexes, confirmed this rate, which was about three times smaller than the rate of complexes in solution. This assay also showed that the pattern of pause sites and the termination site were affected by the surface. By using the Einstein-Sutherland friction-diffusion relation the loading force experienced by RNAP due to DNA-surface friction is estimated and discussed.

Adsorption↗

PubMed1999

Cold injury in mice: a model to study mechanisms of brain edema and neuronal apoptosis.

Small rodents, mice in particular, have been widely used for genetic manipulation because of the extensive knowledge in development, embryology and other molecular aspects of this species. However, the use of mice for neurobiology research in the area of brain edema and neuronal injury has not been common. Here we summarize the studies of cold injury-induced brain edema and neuronal apoptosis using mice. Blood-brain barrier (BBB) permeability, demonstrated by extravasation of a serum albumin tracer, Evans Blue, was increased immediately after the injury and returned to the control level by 24 hr. Water content was maximized at 24 hr, whereas a secondary lesion gradually progressed up to 72 hr after cold injury. The mechanism of the development of the cold injury-induced edema and the secondary lesion, involving of oxygen radicals in particular, was determined using superoxide dismutase (SOD)-1 transgenic (Tg) mice with overexpressed copper, zinc-SOD. All of the parameters, BBB permeability, water content and secondary lesion, were attenuated in the Tg mice as compared to littermate non-Tg mice. This clearly demonstrates that oxygen radicals, superoxide anion in particular, mediate cold injury. We also studied whether apoptosis contributes to brain injury following cold injury. Staining with terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling showed the apoptotic cells widespread throughout the entire lesion while still remaining in the margin. DNA laddering was exhibited by gel electrophoresis. These studies indicate that oxidative mediates the development of cold injury-induced edema and the secondary injury, and induces apoptotic cell death. We believe that cold injury in mice provides a simple animal model to study the pathogenesis of brain edema and apoptosis in genetically altered animals.

Animals↗

PubMed1999

D-RNA molecules associated with subisolates of the VT strain of citrus tristeza virus which induce different seedling-yellows reactions.

Citrus tristeza virus (CTV) strains were previously catalogued as seedling-yellows (SY) and non-SY (nSY) types, according to their yellowing and stunting effects on indicator seedlings. Among subisolates of the VT strain, which were selected from chronically infected Alemow plants, there was a correlation between the presence of 2.4-, 2.7- and 4.5-kb D-RNAs, and SY and nSY reactions, respectively. Similarly, plants infected with Mor-T subisolates, which cause SY, contained D-RNAs of 2.6 to 2.8 kb, while nSY subisolates from recovered sour orange tissue contained a major D-RNA of 5.1 kb. Plants harboring the 2.7-kb D-RNA were protected against challenge inoculation with a subisolate harboring the 4.5-kb D-RNA. This study suggests that the nSY reaction results either from the absence of SY gene(s) in the genomes of certain CTV strains or through the suppression of the effects of SY gene(s) by D-RNAs with 5' parts larger than 4000nt.

Citrus↗

PubMed1999

Adenovirus-mediated interleukin-12 gene therapy for prostate cancer: suppression of orthotopic tumor growth and pre-established lung metastases in an orthotopic model.

Interleukin-12 (IL-12) can elicit potent antitumoral effects that involve the recruitment of specific immune effector cells. We investigated the efficacy of a single injection of a recombinant adenovirus expressing murine IL-12 (AdmIL-12) directly into orthotopic mouse prostate carcinomas generated from a poorly immunogenic cell line (RM-9) derived from the mouse prostate reconstitution system. Significant growth suppression (> 50% reduction of tumor weight) and increased mean survival time (23.4 to 28.9 days) were observed compared with controls. Suppression of pre-established lung metastases was also observed following the injection of AdmIL-12 into the orthotopic tumor. Cytolytic natural killer cell activity was markedly enhanced 1-2 days after virus injection. Immunohistochemical analysis showed significantly elevated intratumoral infiltration of CD4+ and CD8+ T cells 7 days after virus injection. However, splenocyte-derived cytotoxic T lymphocytes were not detected during the 14 days following treatment. Increased numbers of nitric oxide synthase-positive macrophages were seen in the AdmIL-12 treated group 7 days following injection. Systemic inhibition of natural killer cells with antiasialo-GM1 serum led to increased numbers of lung metastases in AdmIL-12-treated orthotopic tumors but did not affect local tumor growth. In this model system the antitumor effects of a single injection of adenovirus-mediated IL-12 appears to be based to a large extent on the activation of nitric oxide synthase in macrophages and possibly T cell activities, whereas the relatively early cytolytic activity of natural killer cells are largely but not exclusively responsible for the antimetastatic effects.

Adenoviridae↗

PubMed1999

The translocation-associated tox1 locus of Cochliobolus heterostrophus is two genetic elements on two different chromosomes.

Previously, Tox1 was defined as a single genetic element controlling the difference between races of Cochliobolus heterostrophus: race T is highly virulent on T-cytoplasm corn and produces the polyketide T-toxin; race O is weakly virulent and does not produce T-toxin. Here we report that Tox1 is two loci, Tox1A and Tox1B, on two different chromosomes. Evidence for two loci derives from: (1) the appearance of 25% Tox+ progeny in crosses between induced Tox1(-) mutants, one defective at Tox1A, the other at Tox1B; (2) the ability of Tox1A- + Tox1B- heterokaryons to complement for T-toxin production; and (3) electrophoretic karyotypes proving that Tox1(-) mutations are physically located on two different chromosomes. Data showing Tox1 as a single genetic element are reconciled with those proving it is two loci by the fact that Tox1 is inseparably linked to the breakpoints of a reciprocal translocation; the translocation results in a four-armed linkage group. In crosses where the translocation is heterozygous (i.e., race T by race O), all markers linked to the four-armed intersection appear linked to each other; in crosses between induced Tox1(-) mutants, complications due to the translocation are eliminated and the two loci segregate independently.

Ascomycota↗

PubMed1999

Simultaneous blood oxygenation level-dependent and cerebral blood flow functional magnetic resonance imaging during forepaw stimulation in the rat.

The blood oxygenation level-dependent (BOLD) contrast mechanism can be modeled as a complex interplay between CBF, cerebral blood volume (CBV), and CMRO2. Positive BOLD signal changes are presumably caused by CBF changes in excess of increases in CMRO2. Because this uncoupling between CBF and CMRO2 may not always be present, the magnitude of BOLD changes may not be a good index of CBF changes. In this study, the relation between BOLD and CBF was investigated further. Continuous arterial spin labeling was combined with a single-shot, multislice echo-planar imaging to enable simultaneous measurements of BOLD and CBF changes in a well-established model of functional brain activation, the electrical forepaw stimulation of alpha-chloralose-anesthetized rats. The paradigm consisted of two 18- to 30-second stimulation periods separated by a 1-minute resting interval. Stimulation parameters were optimized by laser Doppler flowmetry. For the same cross-correlation threshold, the BOLD and CBF active maps were centered within the size of one pixel (470 microm). However, the BOLD map was significantly larger than the CBF map. Measurements taken from 15 rats at 9.4 T using a 10-millisecond echo-time showed 3.7 +/- 1.7% BOLD and 125.67 +/- 81.7% CBF increases in the contralateral somatosensory cortex during the first stimulation, and 2.6 +/- 1.2% BOLD and 79.3 +/- 43.6% CBF increases during the second stimulation. The correlation coefficient between BOLD and CBF changes was 0.89. The overall temporal correlation coefficient between BOLD and CBF time-courses was 0.97. These results show that under the experimental conditions of the current study, the BOLD signal changes follow the changes in CBF.

Animals↗

PubMed1999

Hodgkin's disease: immunoglobulin heavy and light chain gene rearrangements revealed in single Hodgkin/Reed-Sternberg cells.

AIM: To corroborate and investigate the nature of Hodgkin/Reed-Sternberg cells (H/R-S) of various subtypes of Hodgkin's disease. METHOD: Single H/R-S cells were micro-picked from frozen sections of tissues affected by Hodgkin's disease. The DNA from these cells was amplified by the polymerase chain reaction (PCR) with immunoglobulin heavy chain (IgH) gene FRIIIa/JH primers and light chain gene family specific primers. RESULTS: Fifty two of 135 isolated cells gave specific reaction products (36%). IgH and V kappa 4 gene rearrangements were found repeatedly in many H/R-S cells from one case of lymphocyte predominant Hodgkin's disease. Repeated V kappa 4 and individual IgH/V kappa 4,2 rearrangements were seen in one case, and individual IgH and V lambda 3/V kappa 4 rearrangements were seen in another case of nodular sclerosis-type Hodgkin's disease. Repeated IgH/V lambda 3 and individual V lambda 2,4 rearrangements, repeated V kappa 4 and individual IgH/V kappa 3 rearrangements, and repeated IgH and individual V kappa 3/V kappa 4 rearrangement were detected, respectively, in three cases of mixed cellularity-type Hodgkin's disease. Repeated and individual IgH rearrangements were found in another two cases of mixed cellularity-type Hodgkin's disease. CONCLUSION: The H/R-S cells isolated from lymphocyte predominant Hodgkin's disease had IgH and V kappa 4 gene rearrangements, which supports the conclusion that this disease results from a proliferation of neoplastic B cells. The IgH and kappa and/or lambda gene rearrangements seen in H/R-S cells isolated from classic Hodgkin's disease (mixed cellularity-type and nodular sclerosis-type) support the theory that these cells derive from B lineage cells at various stages of differentiation. To our knowledge, this is first time that lambda gene rearrangements have been detected in H/R-S cells.

Electrophoresis, Polyacrylamide Gel↗

PubMed1999

An alpha-cardiac myosin heavy chain gene mutation impairs contraction and relaxation function of cardiac myocytes.

Left Ventricular (LV) myocytes were isolated from 15-wk-old male mice bearing the Arg403 --> Gln alpha-cardiac myosin heavy chain missense mutation (alpha-MHC403/+), a model of familial hypertrophic cardiomyopathy. LV myocytes were classified morphologically: type I, rod shaped with parallel myofibrils; type II, irregularly shaped, shorter and wider than wild-type (WT) control cells, with parallel myofibrils; and type III, irregularly shaped with disoriented myofibrils. Compared with WT myocytes, alpha-MHC403/+ myocytes had fewer type I cells (WT = 74 +/- 3%, alpha-MHC403/+ = 41 +/- 4%, P < 0.01) and more type III cells (WT= 12 +/- 3%, alpha-MHC403/+ = 49 +/- 7%, P < 0.01). In situ histology also demonstrated marked myofibrillar disarray in the alpha-MHC403/+ hearts. With the use of video edge detection, myocytes were paced at 1 Hz (37 degrees C) to determine the effects of the mutation on myocyte function. End-diastolic length was reduced in mutant myocytes, but fractional shortening (% contraction) and sarcomere length were not. Velocity of contraction (-dL/dtmax) was depressed in mutant cells, but more in type II and III cells (-31%) than in type I cells (-18%). Velocity of relaxation (+dL/dt) was also depressed more in type II and III cells (-38%) than in type I cells (-16%). Using fura 2 dye with intracellular Ca2+ transients, we demonstrated that in alpha-MHC403/+ myocytes, the amplitude of the Ca2+ signal during contraction was unchanged but that the time required for decay of the signal to decrease 70% from its maximum was delayed significantly (WT = 159 +/- 8 ms; alpha-MHC403/+ = 217 +/- 14 ms, P < 0.01). Sarco(endo)plasmic reticulum Ca2+-ATPase mRNA levels in alpha-MHC403/+ and WT mice were similar. These data indicate that the altered cardiac dysfunction of alpha-MHC403/+ myocytes is directly due to defective myocyte function rather than to secondary changes in global cardiac function and/or loading conditions.

Action Potentials↗

PubMed1999

Nitric oxide is the predominant mediator of cerebellar hyperemia during somatosensory activation in rats.

Crus II is an area of the cerebellar cortex that receives trigeminal afferents from the perioral region. We investigated the mechanisms of functional hyperemia in cerebellum using activation of crus II by somatosensory stimuli as a model. In particular, we sought to determine whether stimulation of the perioral region increases cerebellar blood flow (BFcrb) in crus II and, if so, whether the response depends on activation of 2-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-kainate receptors and nitric oxide (NO) production. Crus II was exposed in anesthetized rats, and the site was superfused with Ringer. Field potentials were recorded, and BFcrb was measured by laser-Doppler flowmetry. Crus II was activated by electrical stimulation of the perioral region (upper lip). Perioral stimulation evoked the characteristic field potentials in crus II and increased BFcrb (34 +/- 6%; 10 Hz-25 V; n = 6) without changing arterial pressure. The BFcrb increases were associated with a local increase in glucose utilization (74 +/- 8%; P < 0.05; n = 5) and were attenuated by the AMPA-kainate receptor antagonist 2, 3-dihydroxy-6-nitro-7-sulfamoylbenzo-[f]quinoxaline (-71 +/- 3%; 100 microM; P < 0.01; n = 5). The neuronal NO synthase inhibitor 7-nitroindazole (7-NI, 50 mg/kg; n = 5) virtually abolished the increases in BFcrb (-90 +/- 2%; P < 0.01) but did not affect the amplitude of the field potentials. In contrast, 7-NI attenuated the increase in neocortical cerebral blood flow produced by perioral stimulation by 52 +/- 6% (P < 0.05; n = 5). We conclude that crus II activation by somatosensory stimuli produces localized increases in local neural activity and BFcrb that are mediated by activation of glutamate receptors and NO. Unlike in neocortex, in cerebellum the vasodilation depends almost exclusively on NO. The findings underscore the unique role of NO in the mechanisms of synaptic function and blood flow regulation in cerebellum.

Animals↗

PubMed1999

mdm-2 expression correlates with wild-type p53 status in esophageal adenocarcinoma.

Several immunohistochemical studies showed that p53 protein is expressed in 50 to 80% of esophageal adenocarcinomas (EAs). Mutations of this tumor suppressor gene are present in 40 to 70% of EAs, so it is possible that p53 expression might occur as a result of mechanisms other than gene mutation. The human homologue of the murine double minute-2 gene (mdm-2) is a known regulator of p53 activity, and its expression results in stabilization of the wild-type p53 protein and loss of its tumor suppressor function. In this study, we evaluated the frequency of mdm-2 amplification and expression in EA and investigated the relationship between mdm-2 expression and p53 mutation. Thirty-three resection specimens of EAs and associated Barrett's esophagus were evaluated by immunohistochemical methods for p53 and mdm-2 expression. Sixteen of these cases were also evaluated for p53 mutations with use of polymerase chain reaction, single-strand conformational polymorphism, and DNA sequencing and for mdm-2 amplification with a differential polymerase chain reaction-based amplification analysis. Overexpression of p53 was present in 23 EAs (70%), and 18 EAs (55%) overexpressed mdm-2. p53 mutation was observed in 7 (43%) of 16 cases, whereas mdm-2 gene amplification was not detected in any. To summarize, we found substantial discordance of p53 immunohistochemical features and mutation in EA. Significant expression of mdm-2 occurred only in cases with wild-type p53, whereas all of the cases with p53 mutation showed little if any expression of mdm-2. Also, mdm-2 expression in cases with p53 overexpression but without p53 mutation exceeded mdm-2 expression in cases with p53 overexpression and p53 gene mutation. In cases without p53 mutation, overexpression of mdm-2 occurred in 50% of cases and might be responsible for stabilization of p53 protein and possible loss of tumor suppressor function.

Adenocarcinoma↗

PubMed1999

Levels of expression of p27KIP1 protein in human prostate and prostate cancer: an immunohistochemical analysis.

p27KIP1 is a member of the CIP/KIP family of cyclin-dependent kinase inhibitory proteins that negatively regulate cell proliferation. Recent studies reported decreased p27 expression in breast and colon carcinomas and found that the loss of p27 is associated with a poor prognosis. We report here the results of our immunohistochemical analysis of p27 in human prostate cancer. Formalin-fixed, paraffin-embedded, whole-mount sections of prostate cancer from 73 selected patients treated by radical retropubic prostatectomy were obtained from the Department of Pathology, The Methodist Hospital, Houston, Texas. Ten histologically normal and nine high-grade prostatic intraepithelia neoplasia foci were selected from these whole-mount sections, and nine cases of transplant donor prostates were chosen as controls. Also, 10 prostate cancer metastatic lymph nodes were used to compare with the primary cancer group. Sections were immunostained with a monoclonal antibody against p27 protein using the avidin-biotin complex immunohistochemical method. Immunoactivity was evaluated without knowledge of follow-up and recorded as the p27 labeling index (LI) (defined as the percentage of p27-positive cells among epithelia of the same category). The p27 (LI) in normal prostatic epithelia was 86.4+/-3.5% (the mean +/- the standard error of the mean). In contrast, the p27 immunoreactivity was significantly lower in cancers (LI: 43.5 +/-3.7%, P < .001) and in the high-grade prostatic intraepithelial neoplasia group (LI: 59.3 +/- 3.2%, P < .05). Expression of p27 in the metastatic lymph node group was significantly lower than in the other groups, including the prostate cancer cases and the cases of high-grade intraepithelial neoplasia (LI, 7.0%; P = .05). There was no association of the mean p27 LI with progression after radical prostatectomy. Nonrecurrent cases, with a mean follow-up time of greater than 5 years (n = 45), equalled 41.9%; recurrent cases, with a mean follow-up time of 18.3 months (n = 28), equalled 40.0%. The mean p27 LI was not associated with pathologic stage. Organ-confined specimens (n = 21) equalled 34.2%; cases of extraprostatic extension (n = 24) equalled 46.5%; and samples showing seminal vesicle involvement (n = 14) equalled 47.6%. In 14 cases with lymph node metastases, the mean p27 LI was 48.1% in the primary cancer (P = .2322). There was no association of the mean p27 LI with the Gleason score (P = .4747) nor with the clinical stage (P = .9914).

Cell Cycle Proteins↗

PubMed1999

Cloning of Schistosoma japonicum Chinese strain 22.6kD membrane-associated protein (Sj-22.6) gene and its overproduction on Escherichia coli.

A 567bp DNA fragment was amplified from Schistosoma japonicum adult worm mRNA by RT-PCR. Sequence analysis revealed that this fragment contained S. Japonicum Chinese strain membrane-associated protein (Sj-22.6) gene. Then this gene was cloned into the expression vector pGEX-4T, and subsequently expressed in Escherichia coli. The recombinant GST-fusion protein was purified by glutathione agarose affinity chromatography. Its molecular weight was about 48 kD. The yield of expression was around 40 mg/L E.coli culture. The immunological test suggested that the recombinant protein had good antigenity which could make a good basis for the research of its immunological function in Schistosomiasis.

Animals↗

PubMed1999

Production of chimeric antibody in cells and larvae of silkworm.

By using the recombinant baculovirus expression system, the chimeric antibody against human small cell lung carcinoma was expressed in the cells and larvae of silkworm Bomyx mori N (BmN). The chimeric antibodies produced in BmN cells and larvae which were infected with recombinant viruses rNPVL2, rNPVH17 and dual-recombinant virus rNPVLH19 were detected by Western blot analysis. The co-expression products of heavy- and light-chain genes in silkworm larvae revealed stronger immune binding activity than the single product of heavy or light chain gene expression.

Animals↗