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Biomedical subjects

Y X Ma

Publications and source records attributed to Y X Ma.

At least 19 recordsLinked to original sources
PubMed2006

Effect of stachyose supplementation on growth performance, nutrient digestibility and caecal fermentation characteristics in broilers.

1. The objective of this study was to evaluate whether the oligosaccharide stachyose enhances gastrointestinal tract health by fermentation and proliferation of desirable bacteria species and thus affects growth performance and nutrient digestibility in broilers. 2. A total of 432 1-d-old male Arbor Acres (AA) broilers were randomly allocated to one of 6 treatments, with 12 replicate pens per treatment and 6 birds per pen. Chicks were fed a maize-hamlet protein 300 (HP300) basal diet with 0, 4.0, 8.0, 12.0 or 16.0 g/kg stachyose. A sixth diet contained no HP300 but soybean meal (SBM) and provided 8.7 g/kg stachyose and 3.1 g/kg raffinose. The duration of the study was 42 d. 3. Stachyose contents above 12.0 g/kg depressed group body weights, average daily gain and feed/gain but not feed intake during the whole experimental period. Broiler growth decreased linearly and quadratically with increasing stachyose content. No differences were detected between diets supplemented with 12.0 g/kg stachyose and SBM. 4. Nutrient digestibility tended to decrease but not significantly with increasing stachyose. 5. Stachyose content had no significant positive effects on caecal pH, microflora population and the resulting short-chain fatty acid (SCFA) metabolites during the 42 d experiment, with only butyrate differing significantly in the initial period.

Animal Feed↗
PubMed2006

Effects of feed particle size and feed form on survival of Salmonella typhimurium in the alimentary tract and cecal S. typhimurium reduction in growing broilers.

An in vitro experiment and an in vivo experiment were conducted to investigate the effects of feed particle size (coarse and fine) and feed form (mash and pellet) on the survival of Salmonella typhimurium (ST) in the alimentary tract, and the reduction of cecal ST in growing broilers in a 2 x 2 factorial design. All diets in the 2 trials were corn and soybean meal-based diets that differed only in physical characteristics. Diets were provided for birds from d 1 to 22 of age. In the in vitro trial, the relative gizzard weight was lower in birds that were fed the pellet diet (P < 0.01), whereas the relative weight of the cecum was higher in these birds (P < 0.01). Broilers receiving the pellet diet had enhanced concentrations of volatile fatty acids in contents from both the gizzards and the ceca. In addition, there was an increase in gizzard pH (P < 0.01) with the pellet diet, but a reduction in cecal pH (P < 0.05). Pellet-fed birds showed a significantly decreased and increased in vitro death rate of ST in the contents from gizzards (P < 0.01) and ceca (P < 0.05), respectively. A higher in vitro ST death rate in the gizzard was observed in birds given the coarse mash diet compared with those given the fine mash diet. In the in vivo experiment, cecal volatile fatty acid concentrations were increased, whereas cecal pH was decreased significantly (P < 0.05) when birds were fed the pellet diet compared with the mash diet. Furthermore, cecal ST concentrations were higher (P < 0.05) in broilers fed the pellet diet than in those fed the mash diet. Results indicated that the pellet diet increases the incidence of ST in gizzards and ceca in growing broilers and provide evidence demonstrating that the gizzard may play a critical role in reducing ST contamination in growing broilers.

Animal Feed↗
PubMed2004

CMV enhancer/human PDGF-beta promoter for neuron-specific transgene expression.

Using cell-type-specific promoters to restrict expression of therapeutic genes to particular cells is an attractive approach for gene therapy, but often hindered by inefficient transcriptional activities of the promoters. Knowing the enhancer for the human cytomegalovirus (CMV) immediate-early gene improves activities of several cell-type- or tissue-type-specific promoters, we set out to investigate whether it improves neuronal transgene expression driven by a neuron-specific promoter, the platelet-derived growth factor B-chain (PDGF-beta) promoter. A hybrid promoter was constructed by appending a 380-bp fragment of the CMV enhancer 5' to the PDGF-beta promoter. The plasmid containing the promoter was complexed with polyethylenimine for in vitro and in vivo gene transfer. In cultured cells, the plasmid with the hybrid promoter significantly augmented expression of a luciferase reporter gene, providing expression levels 8- to 90-fold and 7- to 178-fold higher than those from two baseline constructs containing the PDGF-beta promoter alone and the CMV enhancer alone, respectively. In particular, the activities of the hybrid promoter in two neural cell lines were close to or higher than that of the CMV immediate-early gene enhancer/promoter, a transcriptional control element that has been considered to be the most robust one identified thus far. After stereotaxic injection into the hippocampus and striatum in rats, the hybrid promoter displayed a neuronal specificity, driving gene expression almost exclusively in neurons. Transgene expression in the brain driven by the hybrid promoter was detectable 24 h after injection, being 10-fold higher than that driven by the PDGF-beta promoter alone. The expression peaked around 5 days at 1.5 x 10(5) relative light units per brain and lasted for at least 4 weeks. This differed strikingly from the expression driven by the PDGF-beta promoter, which was no longer detectable on day 3. The new gene regulatory construct reported in this study will be useful to improve neuronal transgene expression required for gene therapy of neurological disorders and functional studies of the nervous system.

Animals↗
PubMed2004

CNS gene transfer mediated by a novel controlled release system based on DNA complexes of degradable polycation PPE-EA: a comparison with polyethylenimine/DNA complexes.

Nonviral gene delivery systems based upon polycation/plasmid DNA complexes are quickly gaining recognition as an alternative to viral gene vectors for their potential in avoiding immunogenicity and toxicity problems inherent in viral systems. We investigated in this study the feasibility of using a controlled release system based on DNA complexed with a recently developed polymeric gene carrier, polyaminoethyl propylene phosphate (PPE-EA), to achieve gene transfer in the brain. A unique feature of this gene delivery system is the biodegradability of PPE-EA, which can provide a sustained release of DNA at different rates depending on the charge ratio of the polymer to DNA. PPE-EA/DNA complexes, naked DNA, and DNA complexed with polyethylenimine (PEI), a nondegradable cationic polymer known to be an effective gene carrier, were injected intracisternally into the mouse cerebrospinal fluid. Transgene expression mediated by naked DNA was mainly detected in the brain stem, a region close to the injection site. With either PPE-EA or PEI as a carrier, higher levels of gene expression could be detected in the cerebral cortex, basal ganglia, and diencephalons. Transgene expression in the brain mediated by PPE-EA/DNA complexes at an N/P ratio of 2 persisted for at least 4 weeks, with a significant higher level than that produced by either naked plasmid DNA or PEI/DNA at the 4-week time point. Furthermore, PPE-EA displayed much lower toxicity in cultured neural cells as compared to PEI and did not cause detectable pathological changes in the central nervous system (CNS). The results established the potential of PPE-EA as a new and biocompatible gene carrier to achieve sustained gene expression in the CNS.

Animals↗
PubMed2003

Polyethylene glycol modified polyethylenimine for improved CNS gene transfer: effects of PEGylation extent.

Poor solubility of polycation complexes with DNA is one drawback for their in vivo use as gene delivery systems. PEGylation often can improve the solubility of the complexes, minimize their aggregation and reduce their interaction with proteins in the physiological fluid. We investigated in vivo application of polyethylene glycol (PEG) modified polyethylenimine (PEI) for gene expression in the central nervous system. Varied numbers of linear PEG (2 kDa) were grafted to branched PEI (25 kDa) from the average number of PEG per one PEI macromolecule at 1-14.5. While higher degrees of PEG grafting did not improve gene expression, a PEI conjugate with one segment of PEG was able to mediate transgene expression in the spinal cord up to 11-fold higher than PEI homopolymer after intrathecal administration of its DNA complexes into the lumbar spinal cord subarachnoid space. Improved gene expression with this conjugate was observed as well in the brain after the lumbar injection. As assessed in in vitro studies, the PEI conjugate with a low degree of PEG grafting was able to reduce the size of polymer DNA complexes, prevent the aggregation of complexes, decrease the interactions of the complexes with serum proteins, counter the inhibition of serum to gene transfer, and enhance transfection efficiency, although not significant in affecting complex formation and reducing in vitro cell toxicity of PEI. The study provides the in vivo evidence that an appropriate degree of PEG modification is decisive in improving gene transfer mediated by PEGylated polymers.

Animals↗
PubMed2003

Repeated intrathecal administration of plasmid DNA complexed with polyethylene glycol-grafted polyethylenimine led to prolonged transgene expression in the spinal cord.

Gene delivery into the spinal cord provides a potential approach to the treatment of spinal cord traumatic injury, amyotrophic lateral sclerosis, and spinal muscular atrophy. These disorders progress over long periods of time, necessitating a stable expression of functional genes at therapeutic levels for months or years. We investigated in this study the feasibility of achieving prolonged transgene expression in the rat spinal cord through repeated intrathecal administration of plasmid DNA complexed with 25 kDa polyethylenimine (PEI) into the lumbar subarachnoid space. With a single injection, DNA/PEI complexes could provide transgene expression in the spinal cord 40-fold higher than naked plasmid DNA. The transgene expression at the initial level persisted for about 5 days, with a low-level expression being detectable for at least 8 weeks. When repeated dosing was tested, a 70% attenuation of gene expression was observed following reinjection at a 2-week interval. This attenuation was associated with apoptotic cell death and detected even using complexes containing a noncoding DNA that did not mediate any gene expression. When each component of the complexes, PEI polymer or naked DNA alone, were tested in the first dosing, no reduction was found. Using polyethylene glycol (PEG)-grafted PEI for DNA complexes, no attenuation of gene expression was detected after repeated intrathecal injections, even in those rats receiving three doses, administered 2 weeks apart. Lumbar puncture is a routine and relatively nontraumatic clinical procedure. Repeated administration of DNA complexed with PEG-grafted PEI through this less invasive route may prolong the time span of transgene expression when needed, providing a viable strategy for the gene therapy of spinal cord disorders.

Animals↗
PubMed2001

Mutant BRCA1 genes antagonize phenotype of wild-type BRCA1.

Unregulated expression of wild-type BRCA1 (wtBRCA1) confers an altered phenotype in cultured human prostate cancer cells, characterized by chemosensitivity, susceptibility to apoptosis, decreased DNA repair activity, and alterations of key cell regulatory proteins. We now report that the expression of truncated or mutant full-length BRCA1 genes can abrogate certain phenotypic characteristics and/or confer the opposite phenotype to the wild-type BRCA1 gene. In particular, several carboxyl-terminal truncated BRCA1 proteins conferred chemoresistance, decreased susceptibility to apoptosis, and decreased ability to suppress in vivo tumor growth. These truncated BRCA1 proteins also blocked the ability of ectopically expressed wtBRCA1 to induce chemosensitivity and to inhibit estrogen receptor transcriptional activity. Studies using epitope-tagged truncated proteins confirmed their expression, nuclear localization, and functionality. On the other hand, in cells with no endogenous wild-type BRCA1 (HCC1937 human breast cancer cells), the wtBRCA1 gene enhanced cellular DNA repair activity and rendered the cells resistant to DNA damage; while truncated BRCA1 proteins blocked the wtBRCA1-induced chemoresistance. Our findings suggest that truncated BRCA1 proteins can inhibit the function of wild-type BRCA1. They raise the possibility that some inherited BRCA1 mutations may actively promote oncogenesis by blocking the function of the remaining wild-type BRCA1 allele, although this hypothesis remains to be proved.

Apoptosis↗
PubMed2001

The structure dependent electrochemical-response of novel 1-(4-mercaptobutyl)-4-(2-ferrocenylvinyl)pyridinium bromide SAMs on an au electrode.

The 1-(4-mercaptobutyl)-4-(2-ferrocenylvinyl)pyridinium bromide (1-HS(CH2)(4)-4-[(E)-FcCH=CH]C5H4N)+Br- and its hydrogenated product [1-HS(CH2)(4)-4-(-FcCH2CH2)C5H4N]+Br- were synthesized and assembled on an Au electrode to form self-assembled monolayers which showed a structure-dependent electrochemical-response in phosphate buffer aqueous solutions (pH = 7).

Journal Article↗
PubMed2001

Disruption of BRCA1 LXCXE motif alters BRCA1 functional activity and regulation of RB family but not RB protein binding.

The tumor suppressor activity of the BRCA1 gene product is due, in part, to functional interactions with other tumor suppressors, including p53 and the retinoblastoma (RB) protein. RB binding sites on BRCA1 were identified in the C-terminal BRCT domain (Yarden and Brody, 1999) and in the N-terminus (aa 304-394) (Aprelikova et al., 1999). The N-terminal site contains a consensus RB binding motif, LXCXE (aa 358-362), but the role of this motif in RB binding and BRCA1 functional activity is unclear. In both in vitro and in vivo assays, we found that the BRCA1:RB interaction does not require the BRCA1 LXCXE motif, nor does it require an intact A/B binding pocket of RB. In addition, nuclear co-localization of the endogenous BRCA1 and RB proteins was observed. Over-expression of wild-type BRCA1 (wtBRCA1) did not cause cell cycle arrest but did cause down-regulation of expression of RB, p107, p130, and other proteins (e.g., p300), associated with increased sensitivity to DNA-damaging agents. In contrast, expression of a full-length BRCA1 with an LXCXE inactivating mutation (LXCXE-->RXRXH) failed to down-regulate RB, blocked the down-regulation of RB by wtBRCA1, induced chemoresistance, and abrogated the ability of BRCA1 to mediate tumor growth suppression of DU-145 prostate cancer cells. wtBRCA1-induced chemosensitivity was partially reversed by expression of either Rb or p300 and fully reversed by co-expression of Rb plus p300. Our findings suggest that: (1) disruption of the LXCXE motif within the N-terminal RB binding region alters the biologic function of BRCA1; and (2) over-expression of BRCA1 inhibits the expression of RB and RB family (p107 and p130) proteins.

Amino Acid Motifs↗
PubMed2001

Role of direct interaction in BRCA1 inhibition of estrogen receptor activity.

The BRCA1 gene was previously found to inhibit the transcriptional activity of the estrogen receptor [ER-alpha] in human breast and prostate cancer cell lines. In this study, we found that breast cancer-associated mutations of BRCA1 abolish or reduce its ability to inhibit ER-alpha activity and that domains within the amino- and carboxyl-termini of the BRCA1 protein are required for the inhibition. BRCA1 inhibition of ER-alpha activity was demonstrated under conditions in which a BRCA1 transgene was transiently or stably over-expressed in cell lines with endogenous wild-type BRCA1 and in a breast cancer cell line that lacks endogenous functional BRCA1 (HCC1937). In addition, BRCA1 blocked the expression of two endogenous estrogen-regulated gene products in human breast cancer cells: pS2 and cathepsin D. The BRCA1 protein was found to associate with ER-alpha in vivo and to bind to ER-alpha in vitro, by an estrogen-independent interaction that mapped to the amino-terminal region of BRCA1 (ca. amino acid 1-300) and the conserved carboxyl-terminal activation function [AF-2] domain of ER-alpha. Furthermore, several truncated BRCA1 proteins containing the amino-terminal ER-alpha binding region blocked the ability of the full-length BRCA1 protein to inhibit ER-alpha activity. Our findings suggest that the amino-terminus of BRCA1 interacts with ER-alpha, while the carboxyl-terminus of BRCA1 may function as a transcriptional repression domain. Oncogene (2001) 20, 77 - 87.

BRCA1 Protein↗
PubMed2001

The multisubstrate adapter Gab1 regulates hepatocyte growth factor (scatter factor)-c-Met signaling for cell survival and DNA repair.

Hepatocyte growth factor (scatter factor) (HGF/SF) is a pleiotrophic mediator of epithelial cell motility, morphogenesis, angiogenesis, and tumorigenesis. HGF/SF protects cells against DNA damage by a pathway from its receptor c-Met to phosphatidylinositol 3-kinase (PI3K) to c-Akt, resulting in enhanced DNA repair and decreased apoptosis. We now show that protection against the DNA-damaging agent adriamycin (ADR; topoisomerase IIalpha inhibitor) requires the Grb2-binding site of c-Met, and overexpression of the Grb2-associated binder Gab1 (a multisubstrate adapter required for epithelial morphogenesis) inhibits the ability of HGF/SF to protect MDCK epithelial cells against ADR. In contrast to Gab1 and its homolog Gab2, overexpression of c-Cb1, another multisubstrate adapter that associates with c-Met, did not affect protection. Gab1 blocked the ability of HGF/SF to cause the sustained activation of c-Akt and c-Akt signaling (FKHR phosphorylation). The Gab1 inhibition of sustained c-Akt activation and of cell protection did not require the Gab1 pleckstrin homology or SHP2 phosphatase-binding domain but did require the PI3K-binding domain. HGF/SF protection of parental MDCK cells was blocked by wortmannin, expression of PTEN, and dominant negative mutants of p85 (regulatory subunit of PI3K), Akt, and Pak1; the protection of cells overexpressing Gab1 was restored by wild-type or activated mutants of p85, Akt, and Pak1. These findings suggest that the adapter Gab1 may redirect c-Met signaling through PI3K away from a c-Akt/Pak1 cell survival pathway.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Experimental studies on physiological and morphological aspects of Cysticercus cellulosae in pigs.

Three Small-Ear-Miniature, 3 Landrace-Small-Ear-Miniature, and one Douc-Yorkshire-Landrace pigs were inoculated orally with 100 000 eggs of Zhengzhou strain or 10 000 eggs of Harbin strain of Taenia solium. A total of 3739 cysticerci were recovered from 3 Small-Ear-Miniature and 3 Landrace-Small-Ear-Miniature pigs, giving an infection rate of 85.7% and a cysticercus recovery rate of 1.1%. The predilection sites of Cysticercus cellulosae in descending order were leg muscles, abdominal muscles, thoracic muscles, liver, head muscles, diaphragm, tongue, heart, trachea, and omentum/testes. Except 2 calcified cysticerci in the tongue, 2 in the heart, and 176 in the liver, the remaining cysticerci were all alive. The greatest number of cysticerci per 100 g of muscles or viscera was found in the head muscles, followed by the leg, diaphragm, heart, tongue, thoracic, abdominal, omentum, testes, and trachea. All cysticerci were evaginated in pig's bile after fluid was drawn out from cysticerci, whereas evagination occurred in only 83.2% of those without fluid drawing. In 364 evaginated cysticerci, the mean length and width of scolex, proglottid, and bladder, and diameter of rostellum and sucker were 826 x 747 microm, 5,370 x 1,734 microm, 2,885 x 3,002 microm, 155 microm, and 253 microm, respectively. In the protoscolex, the mean number of segments was 33. Each cysticercus had 2 rows of rostellar hooks on the scolex, and the mean length and width of inner and outer hooks were 151 x 18 microm and 117 x 14 microm, respectively. The number of paired hooks ranged from 10 to 18.

Animals↗
PubMed2001

[Down regulatory effects of platelet factor four (PF4) on total adherence and respiratory burst of human neutrophil].

OBJECTIVE: The effect of platelet factor four (PF4) on human neutrophil function was studied. METHODS: Crystal violet dye staining, immunofluorescence labeling, PKC kit assay, NBT and HVA fluoro-spectrophotometry were applied to study the effect of PF4 on total adherence, integrin CD11b level, PKC level and respiratory burst level of resting human neutrophils and FMLP/or PMA-stimulated human neutrophils. RESULTS: It was found that PF4 slightly increased the total adherence of resting human neutrophils. There was no change on integrin CD11b level and respiratory burst level of resting human neutrophils after interaction with PF4. However, PF4 significantly down-regulated the total adherence, integrin CD11b level and respiratory burst level of human neutrophils stimulated by FMLP/or PMA. In addition, PF4 did not influence PKC level on resting and activated human neutrophil. CONCLUSION: These results indicate that PF4 plays a down regulation of the function of human neutrophils. Differing from other members of classical CXC-chemokine family, the signaling of PF4 is not through PLC-PKC signal pathway.

CD11b Antigen↗
PubMed2000

The cytokine hepatocyte growth factor/scatter factor inhibits apoptosis and enhances DNA repair by a common mechanism involving signaling through phosphatidyl inositol 3' kinase.

Scatter factor (SF) [aka. hepatocyte growth factor (HGF)] (designated HGF/SF) is a multifunctional cytokine that stimulates tumor cell invasion and angiogenesis. We recently reported that HGF/SF protects epithelial and carcinoma cells against cytotoxicity from DNA-damaging agents and that HGF/SF-mediated cytoprotection was associated with up-regulation of the anti-apoptotic protein Bcl-XL in cells exposed to adriamycin. We now report that in addition to blocking apoptosis, HGF/SF markedly enhances the repair of DNA strand breaks caused by adriamycin or gamma radiation. Constitutive expression of Bcl-XL in MDA-MB-453 breast cancer cells not only simulated the HGF/SF-mediated chemoradioresistance, but also enhanced the repair of DNA strand breaks. The ability of HGF/SF to induce both chemoresistance and DNA repair was inhibited by wortmannin, suggesting that these activities of HGF/SF are due, in part, to a phosphatidylinositol-3'-kinase (PI3K) dependent signaling pathway. Consistent with this finding, HGF/SF induced the phosphorylation of c-Akt (protein kinase-B), a PI3K substrate implicated in apoptosis inhibition; and an expression vector encoding a dominant negative kinase inactive Akt partially but significantly inhibited HGF/SF-mediated cell protection and DNA repair. These findings suggest that HGF/SF activates a cell survival and DNA repair pathway that involves signaling through PI3K and c-Akt and stabilization of the expression of Bcl-XL; and they implicate Bcl-XL in the DNA repair process.

Antimutagenic Agents↗
PubMed1999

Oncospheres of Taenia solium and T. saginata asiatica develop into metacestodes in normal and immunosuppressed mice.

Normal and immunosuppressed mice were infected with oncospheres of Taenia saginata asiatica and T. solium. Although normal ICR mice were not susceptible to these two parasites, cysticerci were recovered from the immunosuppressed ones following venous injection. For T. s. asiatica, immunosuppressed ICR mice had an infection rate of 12.5% and six cysticerci of this parasite were recovered from three males. After injection of T. solium oncospheres, a high infection rate of 57% was obtained and 23 cysticerci were collected from 13 male immunosuppressed ICR mice. The immunosuppressed C57 mice had the highest infection rate (100%) and cysticercus recovery rate (2.4%) for T. solium. The infection rate and cysticercus recovery rate in six normal C57 mice were 40% and 3% respectively. The immunosuppressed ICR, Balb/c and C3H mice were also susceptible to T. s. asiatica.

Animals↗
PubMed1999

Ultraviolet radiation down-regulates expression of the cell-cycle inhibitor p21WAF1/CIP1 in human cancer cells independently of p53.

PURPOSE: To investigate the regulation of G1 cyclin-dependent kinase inhibitor p21WAF1/CIP1 by ultraviolet (UV) radiation in human carcinoma cells. MATERIALS AND METHODS: Human cancer cell lines were irradiated with UV-C (254 nm) radiation, and their responses were characterized by Western blotting, Northern blotting, semi-quantitative RT-PCR analysis, trypan blue staining and flow cytometric cell cycle analysis. RESULTS: At 24 h after UV irradiation, p21 expression was down-regulated in various cancer cell types (breast, prostrate, cervix, colon, glioma, squamous cancers), independently of their p53 genetic and functional status. UV-mediated down-regulation of p21 was dose- and time-dependent, was observed at the protein and mRNA levels, and did not correlate with cytotoxicity. Reduction of p21 protein levels required about 4 and 1 h, respectively, in MCF-7 and MDA-MB-231 breast cancer cells; some of the UV-induced decreases in p21 levels in these cell lines was due to enhanced proteasomal degradation. Despite decreased p21 levels, UV-irradiated breast cancer cells with wild-type p53 (MCF-7) retained the capacity for G1 cell-cycle arrest, whereas UV-treated cells with mutant p53 (MDA-MB-231) accumulated in S phase, suggesting a p53-dependent G1 checkpoint in MCF-7. UV treatment caused other alterations in cell-cycle regulatory, DNA repair and tumour suppressor genes, as described in this report. CONCLUSIONS: In contrast to X-rays, UV causes down-regulation of the cell-cycle inhibitor p21 in tumour cells. It is postulated that this may be an adaptation to promote the growth and survival of transformed cells.

BRCA2 Protein↗
PubMed1999

Sexual development of Taenia solium in hamsters from rodent-derived cysticerci.

In order to determine whether Taenia solium can be maintained in the laboratory using rodents as definitive hosts, six nude rats, 20 immunosuppressed Mongolian gerbils and 20 immunosuppressed Syrian hamsters were each inoculated through a stomach tube with three cysticerci recovered from SCID mice. No adult worms of T. solium were found in the intestinal tract of any of these 46 rodents. In addition, five immunosuppressed Syrian hamsters were fed with the same number of cysticerci enclosed in rodent muscles from SCID mice. Two of these hamsters were found to be infected 40 days post-infection, each harbouring a sexually developed worm in the intestinal tract. Although no eggs were produced, prepatent infections may be possible if a longer time was allowed for worm development. Moreover, the maintenance of the life cycle of T. solium in the laboratory using the rodent model can be established.

Animals↗