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Biomedical subjects

S H Li

Publications and source records attributed to S H Li.

At least 37 records · Page 2Linked to original sources

[Detection of DNA of Toxoplasma gondii in rat by using polymerase chain reaction].

OBJECTIVE: To study the significance of DNA of Toxoplasma gondii in peripheral blood. METHODS: DNA of T. gondii in peripheral blood of 50 infected rats was detected by polymerase chain reaction. A pair of primers was designed, according to the sequence P30 gene specific to T. gondii, to amplify DNA from T. gondii by PCR. RESULTS: The primers amplified DNA specifically from T. gondii and could not amplify DNA from humans, uninfected rat and mouse and from Trichomonas vaginalis and Entamoeba histolytica. DNA of two Toxoplasma parasites was detected by 35 cycles of amplification, indicating a fair sensitivity of the PCR system. CONCLUSION: PCR may have a value for early diagnosis of T. gondii infection in rat.

Animals↗

[Determination of T lymphocytes and trace elements in spleen from rats infected with Toxoplasma gondii].

OBJECTIVE: To determine the level of five trace elements(Fe2+, Cu2+, Zn2+, Ca2+, Mg2+) in the spleen and changes of T lymphocyte and its subtype variations in peripheral blood from the rats infected with Toxoplasma gondii. METHODS: Twenty rats were randomly and equally divided into two groups: control group and experiment group. Each rat in the experiment group received an i.p. injection of 2 ml normal saline containing 1.5 x 10(6) tachyzoites of T. gondii. On the 64th day after injection of T. gondii, the changes in T lymphocytes (TL) and their subgroups, the helper T lymphocytes (Th) and the suppressor T lymphocytes(Ts) in the peripheral blood of the rats with T. gondii were determined by the assay of the lymphocytes labeled with intercellular acid alpha-naphthyl acetate esterase. All the rats were killed and the atomic absorption method were used for detecting the level of trace elements in the spleen tissue. RESULTS: The number of TL and Th in experiment group was significantly lower than that of control (P < 0.01, P < 0.01). The ratio of Th/Ts showed a significant difference between the two groups. The level of Fe2+, Cu2+ in experiment group was significantly reduced (P < 0.01). The amount of Mg2+ in infected rats was higher than that of the control(P < 0.01). No statistical difference in the content of Zn2+, Ca2+ was found between the two groups. CONCLUSION: T. gondii infection might cause the changes in the TL and Th in peripheral blood and the changes in trace elements in spleen of the rats.

Animals↗

[Comparison of hard tissue changes by treatment of angle class II malocclusion with Kloehn's extraoral arch in periods of transitional dentition and permanent tooth].

OBJECTIVE: The optimal treatment period by use of extraoral arch was understood by comparison of the changes of facial hard tissue in treatment of Angle II malocclusion with Kloehn's extraoral arch and Edgwise appliance. METHODS: A group of 7-8 year old children and a group of 10-11 year-old children were selected, including 16 Angle II malocclusion cases in each group, respectively. Data of cephalograms and model analysis were compared between pretreatment and posttreatment. RESULTS: The more distance of maxillary molar and more obvious inhibition of maxilla bone growth forward in group of 7-8 year-old children (group of transitional dentition) were detected than that in group of 10-11 year-old children(group of permanent tooth). CONCLUSION: More effective treatment by use of extraoral arch was detected in the period of transitional dentition than that in permanent tooth.

English Abstract↗

Intranuclear huntingtin increases the expression of caspase-1 and induces apoptosis.

Expansion of a polyglutamine repeat in huntingtin causes Huntington's disease (HD). Although full-length huntingtin is predominantly distributed in the cytoplasm, N-terminal fragments of huntingtin with expanded polyglutamine tracts are able to accumulate in the nucleus and kill neurons through apoptotic pathways. Transgenic mice expressing N-terminal mutant huntingtin show intranuclear huntingtin accumulation and develop progressive neurological symptoms. Inhibiting caspase-1 can prolong the survival of these HD mice. How intranuclear huntingtin is associated with caspase activation and apoptosis is unclear. Here we report that intranuclear huntingtin induces the activation of caspase-3 and the release of cytochrome c from mitochondria in cultured cells. As a result, cells expressing intranuclear huntingtin undergo apoptosis. We show that intranuclear huntingtin increases the expression of caspase-1, which may in turn activate caspase-3 and trigger apoptosis. We propose that the increased level of caspase-1 induced by intranuclear huntingtin contributes to HD-associated cell death.

Animals↗

6-(18)F-DOPA PET study in patients with schizophrenia. Positron emission tomography.

Presynaptic dopamine metabolism was studied in a group of patients with schizophrenia and in an age- and gender-matched normal control group using 6-[(18)F]fluoro-L-DOPA ((18)F-DOPA) and positron emission tomography (PET). Nineteen patients, nine drug-free, 10 on neuroleptics, and 13 normal control subjects underwent PET scans using (18)F-DOPA. The neuroleptic-treated patients were taking typical neuroleptics (N=4) or the atypical neuroleptic, clozapine (N=6). The ratio of specific/non-specific activity was calculated for eight cortical and subcortical regions of interest. Medication-free patients had a significant reduction in (18)F-DOPA uptake in the ventral striatum (P=0.04) and significantly increased uptake in the posterior cingulate (P=0.02) compared with normal control subjects. The 18F-DOPA PET technique proved to be useful and sensitive in detecting changes in dopamine metabolism in patients with schizophrenia in vivo. The results of this study provide evidence of an aberrant dopamine system in schizophrenia.

Adult↗

Long glutamine tracts cause nuclear localization of a novel form of huntingtin in medium spiny striatal neurons in HdhQ92 and HdhQ111 knock-in mice.

Huntington's disease (HD) is caused by an expanded N-terminal glutamine tract that endows huntingtin with a striatal-selective structural property ultimately toxic to medium spiny neurons. In precise genetic models of juvenile HD, HdhQ92 and HdhQ111 knock-in mice, long polyglutamine segments change huntingtin's physical properties, producing HD-like in vivo correlates in the striatum, including nuclear localization of a version of the full-length protein predominant in medium spiny neurons, and subsequent formation of N-terminal inclusions and insoluble aggregate. These changes show glutamine length dependence and dominant inheritance with recruitment of wild-type protein, critical features of the altered HD property that strongly implicate them in the HD disease process and that suggest alternative pathogenic scenarios: the effect of the glutamine tract may act by altering interaction with a critical cellular constituent or by depleting a form of huntingtin essential to medium spiny striatal neurons.

Animals↗

Expression of huntingtin-associated protein-1 in neuronal cells implicates a role in neuritic growth.

Huntingtin-associated protein-1 (HAP1) binds more tightly to mutant huntingtin, but its function and distribution in neurites are not clear. Using PC12 cells and cultured hippocampal neurons, we found that two HAP1 isoforms, HAP1-A and HAP1-B, have different subcellular localizations. While most HAP1-B is diffusely distributed within the cytoplasm, HAP1-A is enriched in the growth cones and neuritic puncta of developing neurons. In mature neurons and adult brain neurons, however, HAP1-A is concentrated in axon terminals and associated with synaptic vesicles. Transfection of HAP1-A in PC12 cells significantly promotes neurite extension, with HAP1-A distributed in the distal regions of the growing neurites. Cotransfection of mutant huntingtin with HAP1-A in PC12 cells results in the accumulation of HAP1-A on huntingtin aggregates and the inhibition of neurite promotion by HAP1-A. This study suggests that HAP1-A has a function in neuritic development and synaptic function and that mutant huntingtin may alter this function.

Amino Acid Sequence↗

Rearranged taxanes from the bark of Taxus yunnanensis.

Five new 11(15-->1)-abeo-taxane diterpenoids, taxuyunnanines K-O (1-5), were isolated from an ethanol extract of the bark of Taxus yunnanensis, and their structures were determined using MS and NMR techniques. Compounds 1/2 and 4/5 are rearranged taxane diterpenoids possessing an opened oxetane ring moiety at C4(20). Compounds 4/5 are rearranged taxoids lacking an oxygenated functionality at C-4.

Bridged-Ring Compounds↗

Amino-terminal fragments of mutant huntingtin show selective accumulation in striatal neurons and synaptic toxicity.

Huntington disease (HD) is caused by expansion of a glutamine repeat in the amino-terminal region of huntingtin. Despite its widespread expression, mutant huntingtin induces selective neuronal loss in striatal neurons. Here we report that, in mutant mice expressing HD repeats, the production and aggregation of N-terminal huntingtin fragments preferentially occur in HD-affected neurons and their processes and axonal terminals. N-terminal fragments of mutant huntingtin form aggregates and induce neuritic degeneration in cultured striatal neurons. N-terminal mutant huntingtin also binds to synaptic vesicles and inhibits their glutamate uptake in vitro. The specific processing and accumulation of toxic fragments of N-terminal huntingtin in HD-affected striatal neurons, especially in their neuronal processes and axonal terminals, may contribute to the selective neuropathology of HD.

Animals↗

Study of stabilizing CaF2:Dy ultraviolet sensitivity by double annealing treatment.

The intrinsic thermoluminescent response to ultraviolet radiation of CaF2:Dy phosphor is enhanced by pre-irradiation high-temperature annealing treatment. The thermoluminescent response is stabilized by adding a medium temperature annealing treatment after the previous annealing. The experimental results show that the annealing treatment of 1 h 850 degrees C high-temperature annealing followed by 1 h 350 degrees C medium-temperature annealing is the optimum treatment to have high thermoluminescent response and good stability. The results also show that (1) the thermoluminescent response to 253.7 nm ultraviolet radiation is increased and stabilized, (2) the thermoluminescent sensitivity and glow curve distribution to 235.7 nm ultraviolet radiation are retained, and (3) the thermoluminescent response to 253.7 nm ultraviolet is linear from 3 to 1 x 10(3) Jm(-2), but there is no linear response with respect to 365 nm ultraviolet.

Calcium Fluoride↗

Polyphenols from Eriobotrya japonica and their cytotoxicity against human oral tumor cell lines.

Three new flavonoid glycosides, together with 15 known flavonoids, have been isolated from the leaves of Eriobotrya japonica, and characterized as (2S)- and (2R)-naringenin 8-C-alpha-L-rhamnopyranosyl-(1-->2)-beta-D-glucopyranosides, and cinchonain Id 7-O-beta-D-glucopyranoside, respectively, based on spectral analyses including two dimensional (2D) NMR techniques. Higher proanthocyanidin fraction in the water-soluble portion of the extract was characterized as a procyanidin oligomer mixture mainly composed of undecameric procyanidin. These polyphenols have also been assessed for cytotoxic activity against two human oral tumor (human squamous cell carcinoma and human salivary gland tumor) cell lines. Selective cytotoxicity of the procyanidin oligomer between tumor and normal gingival fibroblast cells, and its possible mechanism, were also described.

Antibodies, Monoclonal↗

[Analysis of trace elements in liver, spleen and brain of rats infected with Toxoplasma gondii].

OBJECTIVE: To study the level of five trace elements(Fe2+, Cu2+, Zn2+, Ca2+, Mg2+) in the liver, spleen and brain of the rats infected with Toxoplasma gondii. METHODS: 20 rats were randomly and equally divided into two groups: normal group and experimental group. On the 64th day after injection of 1.5 x 10(6) T. gondii/2 ml, all of the rats were killed and the atomic absorption method were used. RESULTS: Compared with the normal group, the level of Cu2+ in liver in experimental group was significantly reduced (P < 0.01), and the amount of Fe2+ of sick rats were higher than that of the normal (P < 0.01). No differences in the content of Zn2+, Ca2+, Mg2+ between the experimental and control group were determined; the level of Fe2+, Cu2+ in spleen in experimental group was significantly altered (P < 0.01). The amount of Mg2+ of sick rats were higher than that of the normal (P < 0.01), and no difference on the content of Zn2+, Ca2+ between the experimental and control group were estimated; the level of Fe2+, Cu2+, Mg2+ in brain in experimental group was significantly reduced (P < 0.01). The amount of Ca2+ of sick rats were higher than that of the normal (P < 0.02). No difference on the content of Zn2+ between the experimental and control group were estimated. CONCLUSION: T. gondii infection might cause changes in trace elements in the liver, spleen and brain of rats.

Animals↗

Cellular defects and altered gene expression in PC12 cells stably expressing mutant huntingtin.

Expanded polyglutamine tracts cause huntingtin and other proteins to accumulate and aggregate in neuronal nuclei. Whether the intranuclear aggregation or localization of a polyglutamine protein initiates cellular pathology remains controversial. We established stably transfected pheochromocytoma PC12 cells that express the N-terminal fragment of huntingtin containing 20 (20Q) or 150 (150Q) glutamine residues. The 150Q protein is predominantly present in the nuclei, whereas the 20Q protein is distributed throughout the cytoplasm. Electron microscopic examination confirmed that most of the 150Q protein is diffuse in the nucleus with very few microscopic aggregates observed. Compared with parental PC12 cells and cells expressing 20Q, cells expressing 150Q display abnormal morphology, lack normal neurite development, die more rapidly, and are more susceptible to apoptotic stimulation. The extent of these cellular defects in 150Q cells is correlated with the expression level of the 150Q protein. Differential display PCR and expression studies show that cells expressing 150Q have altered expression of multiple genes, including those that are important for neurite outgrowth. Our study suggests that mutant huntingtin in the nucleus is able to induce multiple cellular defects by interfering with gene expression even in the absence of aggregation.

Animals↗

Long-term trend toward earlier breeding in an American bird: a response to global warming?

In regions with severe winters, global warming may be expected to cause earlier onset of breeding in most animals, yet no documentation of such a trend exists in North America. In a study of marked individuals of the Mexican jay (Aphelocoma ultramarina) in southeastern Arizona, from 1971 to 1998, the mean Julian date of first clutch in the population declined significantly by 10.1 days. The date of the first nest in the population also became earlier, by 10.8 days. These changes were associated with significant trends toward increased monthly minimum temperatures on the study area, traits that are associated with the onset of breeding in this population. Significant trends from 1971 to 1997 toward warmer minimum temperatures in the months before and during the initiation of breeding were observed. These trends parallel changes in minimum temperatures and community composition in a recent study of grassland ecology in the western United States. Together, they suggest that more attention should be given to the possible ecological importance of global change in minimum temperatures.

Animals↗

Cloning of novel temperature-related expressed sequence tags in rat testis during spermatogenesis.

Spermatogenesis needs the relatively cool environment of the scrotum in most mammals, it would be arrested when the testis was exposed to abdominal temperature. In this study, we have used a differential display PCR technique (DD-PCR) to screen temperature-related ESTs during spermatogenesis (TRS) in scrotal testes through a unilateral cryptorchid rat model after in situ analysis of testis cell DNA fragmentation. We reported here the cloning and sequencing of three such ESTs: TRS1, TRS3, and TRS4. Northern blot analysis confirmed that they were expressed specifically in scrotal testes. In situ hybridization showed that TRS1 was mainly expressed in the spermatocytes and the round spermatids in scrotal testis. Homology searches revealed that TRS1 and TRS3 were unknown cDNA sequences, and TRS4 was identical to a known EST whose function had not been reported. TRS1, TRS2, and TRS3 were first found to be temperature-related during spermatogenesis.

Animals↗

Various forms of mouse lactoferrins: purification and characterization.

This work was conducted to study the microheterogeneity of mouse lactoferrin (LF). Two forms, LF1 and LF2, could be purified from uterine luminal fluid by ion-exchange HPLC on a Protein PAK SP 5PW column. Another form, LF3, was purified from the epididymis homogenate by affinity chromatography on a column of Protein A-Sepharose coupled with the purified LF2 antibody that was prepared to give no crossreaction with serum albumin. Both LF1 and LF2 showed a Mr 74000 band while LF3 gave a Mr 70000 band on reducing SDS-PAGE. All of them were reduced to a Mr 68000 band after they had been digested with N-glycosidase F. The data from automated Edman degradation confirmed the completely identical 19 amino acid sequences in the N-terminal regions of these three LFs, except the lack of N-terminal Lys-Ala of LF2/LF3 in LF1. LF in tissue homogenates was immunodetected by Western blot procedure using the purified LF2 antibody. Different amounts of LF with a molecular mass of the 70000 or 74000 were distributed in the non-sexual organs such as kidney, spleen, lung, heart and liver and the sexual glands including epididymis, vagina, uterus, ovary and prostate. No LF was detected in stomach, intestine, testis and seminal vesicle.

Amino Acid Sequence↗