Biomedical subjects
Publications and source records attributed to Z Xu.
The morphological characters and commercial identification on Semen Torreyae has been reported. The results of identification of commercial samples indicated that Torreya grandis was mainly used; T. fargesii, T. yunnanensis and T. jackii were used in their producing areas.
OBJECTIVE: To determine the contents and analyze the ingredients of the amino acids in seeds of genus Torreya. METHODS: The amino acid contents and ingredients were determined by amino acid analyzer. RESULTS: There were 19 amino acids in the seeds of T. grandis, T. grandis cv. merrillii, T. yunnanensis, T. jackii and T. fargesii, and their amino acid contents are 9.10%, 9.90%, 5.03%, 7.26% and 6.07% respectively. There were 17 amino acids in the seeds of T. jiulongshanensis, T. nucifera and T. grandis cv. merrillii (baked) and their amino acid contents are 14.11%, 9.87% and 9.22% respectively. tively.
OBJECTIVE: To determine the preventive effect of the oil from the seed of Torreya grandis cv. merrillii (OTM) on experimental atherosclerosis in rats. METHODS: The concentration of blood lipids, plasma thromboxane (TXA2), prostacyclin (PGI2), the ratio of TXA2/PGI2 and endothelin (ET) were investigated in male Wistar rats fed high-fat feed (HFF) containing OTM(2%) for 12 weeks. RESULTS: OTM could reduce the level of serum total cholesterol (TC), triglyceride (TG) and the atherosclerosic index (AI), and increase the level of serum high-density-lipoprotein cholesterol (HDL-C). The plasma concentration of TXA2, ET and the ratio of TXA2/PGI2 in group supplemented with OTM were lower than those in HFF group. Moreover, the level of plasma PGI2, was higher than that in HFF group. CONCLUSION: OTM is beneficial in preventing atherosclerosis.
OBJECTIVE: To evaluate the advantage and applications of pedicled galeal flap in head and neck region. METHODS: A consecutive series of 17 patients underwent surgical reconstruction with pedicled galeal flaps after head and neck tumor resection. The defects included nasopharynx, skull base, maxilla, orbital base, oropharynx and oral cavity and the size ranged from 5 cm x 5 cm to 10 cm x 10 cm. The technique for using this flap was described and application was illustrated with 3 case reports. RESULTS: Complete success of galeal flaps for the reconstruction of head and neck defects was achieved in 13 of the 17 cases (76.5%) and partial necrosis was observed in the remaining 4 cases (23.4%). Immediate wound complications occurred in four cases, which resolved spontaneously. Four delayed complications were observed in 4 of 9 survival cases that included trismus (3) and alopecia (1). CONCLUSION: Galeal flap is a thin, pliable and well vascularised reconstruction tissue and is highly reliable. The donor site morbidity is minor. We have found the flap to be useful in the reconstruction of a variety of defects in head and neck, especially in skull base, orbital base, nasopharynx and oropharynx.
OBJECTIVE: To restore the laryngeal function of laryngectomee. METHODS: From 1990 to 1999, laryngeal reconstructions were performed in 34 cases of laryngectomee. The patients were 33 male, and one female. The age range was 27 to 77 years, with a mean age of 56.6. Thirty-three cases were total laryngectomized, one case due to laryngeal injury. The duration of alaryngeal was 2-72 months, with a mean of 18 months. The characteristic of this operation is that a cervical myocutaneous flap was used to link the pharynx and trachea, to act as an epiglottis. RESULTS: Speech function in all patients was good. One case can breathe through the larynx after decannulation and 13 cases can breath through the larynx in daytime. CONCLUSION: Laryngeal reconstruction for laryngectomee is applicable in laryngeal operation.
OBJECTIVE: The clinical experiment was designed for observing the effects of deliberate hypotension at different level on cerebral blood flow and metabolism. METHODS: 30 ASA Grade I-II patients were randomly allocated to one of three groups (each group n = 10). Hypotension was induced by sodium nitroprusside in group 1[mean arterial pressure (MAP) = 55 mmHg] and group 2 (MAP = 65 mmHg). Group 3 (control) was on normotension. The changes of cerebral blood flow during hypotension were estimated according to the variability of cerebral blood flow velocity (CBFV) in the middle cerebral artery(MCA), which was obtained through transcranial Doppler ultrasonography (TCD). RESULTS: Hypotension caused a moderate decrease in CBFV, but no significant difference, in CBFV and oxygen saturation in internal jugular vein(SjO2), either among three groups or during the procedure. CONCLUSIONS: It is safe for cerebral perfusion and metabolism with deliberate hypotension at MAP = 55 mmHg.
OBJECTIVE: To analyse the histopathology and the factors influencing the outcome of surgical treatment of primary intracerebral neoplasms only presenting with epilepsy. METHODS: 55 patients with primary intracerebral tumors presenting with epilepsy without other neurologic signs were retrospectively reviewed. RESULTS: 54(98.2%) cases were histologically diagnosed as gliomas among which 42(76.4%) were low-grade and 12(21.8%) high-grade. The incidence of complications for tumor removals was 32.7%. Of the 41 patients who had postoperative follow-up more than 6 months after operation, 20(48.8%) were seizure-free, 3 were rare, 4 were improved, and 14 (34.1%) had no appreciable reduction in seizure frequency. The position of the tumors was significantly correlated with the incidence of postoperative complications and the postoperative seizure control (P < 0.05). The incidence of postoperative complications for frontal and parietal tumors was higher than that for temporal tumors, while the temporal tumors had better postoperative seizure control than the frontal and the parietal ones. CONCLUSIONS: Most of the primary intracerebral tumors only presenting with epilepsy were low-grade gliomas. The position of tumors was an important factor influencing the extent of surgical removal and the postoperative seizure control.
FT-Raman spectroscopy was used to investigate 40 normal and malignant tissues from stomach. Statistic analysis shows that the bands related to OH, NH, C=O stretching and H-O-H bending are stronger in malignant tissues. This phenomenon suggests that the hydrogen bonding systems among water and protein vary in malignant tissues.
The infrared and Raman spectra of five isomultinuclear organometallic carbyne compounds were studied. The results show that the introduction of N atom from TMEDA or P atom from DPPE to W atom (both N and P are strong sigma-donor and weak pi-acceptor) will decrease the bonding intensity of W identical to C. The pressure tunning IR and Raman spectra of compound III indicate the presence of pressure-induced phase-transition near 20 kbar in it. There are two effects on the nu (W identical to C) of this compound with increasing pressure: the normal increasing the nu (W identical to C) wavenumber due to the shorting W identical to C bond and increasing the W-CO pi backbonding to decrease the nu (W identical to C) wavenumber.
We propose a new way to reveal structural arrangement of hydrogen bond network using FTIR spectroscopy. When KBr pellet and fluorolube mull methods are used to prepare samples for IR measurements, the resultant spectra sometimes show significant differences, sometimes not. The reason is unknown. We use cryogenic FTIR spectra to prove pressure effect accounts for spectral variation in different sampling process. The sensitivity of the FTIR spectra to external pressure is related to the three-dimensional arrangement of hydrogen bonding network in the sample. When hydrogen bonds are in one plane, they can not resist external pressure applied perpendicular to that plane. Consequently, large differences appear between the spectra obtained using KBr pellet and fluorolube mull methods. On the other hand, when hydrogen bonds orientate towards various directions, the hydrogen bonding system can resist pressure from any directions. Thus, the FTIR spectra exhibit little variation using different sampling methods. We propose that the spectral variation obtained using above methods is a criterion to judge whether the hyrogen bonds orientate toward various directions in three-dimensional space or not.
In this paper we report a simple method for deducing optical constants and thickness from the reflection interference spectrum of a thin transparent film which is on a substrate of high reflection coefficient. When a light beam is incident on the surface of the film, the reflection light beams at the front and rear faces are coherent. We calculated the optical constants and thickness of the film from the reflection spectrum. This simple method makes a directly programmable calculation possible.
Cytotoxic T lymphocytes (CTL) lyse antigen-bearing target cells by two distinct pathways. Whereas granule exocytosis targets any antigen-bearing cell, fas-mediated cytotoxicity kills only fas-expressing cells and does not require antigen expression. Fas pathway activation can potentially lead to lysis of uninfected bystander cells. We examined the relative usage of the two pathways by CTL clones and cell lines directed against four different human immunodeficiency virus (HIV) proteins in lysing primary HIV-infected targets. Although fas was expressed on HIV-infected primary CD4(+) T cells, their lysis by antigen-specific CD8(+) CTL was only by the granule pathway. Fas ligand (fasL) was not detectable on antigen-specific CD8 clones, T-cell lines, or circulating HIV-specific CD8 T cells from HIV-infected donors, stained with a tetrameric HLA-A2-HIV-peptide complex. FasL expression by HIV-specific CTL clones was not activated by exposure to HIV-presenting cells, but was after unphysiological stimulation with phorbol myristate acetate (PMA). CTL clones did not lyse bystander Jurkat cells, but HIV-infected primary CD4(+) T cells lysed uninfected bystander cells by the fas-mediated pathway. These results suggest that HIV-specific CD8(+) CTL do not cause HIV immunopathology by lysing bystander cells. On the contrary, fas-mediated lysis of uninfected cells by HIV-infected cells may contribute to CD4 decline.
A new subdivision with distinctive morphological and functional attributes has been identified at the caudomedial margin of the neostriatum and surrounding the rostrolateral border of the globus pallidus in the brains of the rat, cat, monkey, and human. The subdivision is termed marginal division (MrD) based on its location. It is readily distinguishable from the rest of striatum by consisting of spindle-shaped neurons, special connections, and intensely expressed immunoreactivities of many neuropeptides and some monoamines in the fibers, terminals, and neuronal somata. Three-dimensional reconstruction from Nissl-stained sections of the rat brain revealed that the MrD is a flat, pan-shaped zone between the neostriatum and globus pallidus. Functional neuronal connections were delineated by chemical-induced c-Fos expression between the MrD and hippocampus, amygdala, as well as the basal nucleus of Meynert. In rats with chemical lesions of bilateral MrD, learning and memory functions were severely impaired as demonstrated by double blind Y-maze test. Our results thus suggested that the MrD is a distinct part and a universal structure in the neostriatum of the mammalian brain and might play an important role in the mechanism of learning and memory.
We isolated and characterized a recessive mutant, named dlp1, which shows the Dlp phenotype (delayed loss of proliferation activity) during the autophagic death of cdc28. The dip1 mutant was found to consist of two subtypes of cells based on colony morphology. One subtype with the Dlp phenotype, named dlp1-1, became large, red, and nibbled during the incubation, suggesting that the cells on the surface of the colonies were dying. The other without the Dlp phenotype, named dlp1-s, retained small, white colonies even after a prolonged incubation and was found to be a petite mutant. The change from dlp1-1 to dlp1-s (petite) occurred much more frequently (about 15%) than that from the wild-type to petite mutant (less than 1%). The lifespan of both subtypes of cells was severely shortened. The copy number of the endogenous 2micron plasmid of dlp1-1 was 68-fold that of the original cdc28, and decreased by half after the conversion to dlp1-s (petite). A 4.0-kbp fragment of the 2micron plasmid containing REP2 decreased the copy number of the endogenous 2micron plasmid to 8-fold that of the original cdc28 cells and partially rescued the shortened lifespan, in addition to resulting in the complete complementation of the Dlp and nibbled-colony phenotypes. These results suggest that DLP1 is a chromosomal gene that regulates the copy number of the 2micron plasmid, and that the shortening of the lifespan and other effects of the dlp1 mutation are likely caused by the increased copy number of the endogenous 2micron plasmid.
Vacuole fusion occurs in three stages: priming, in which Sec18p mediates Sec17p release, LMA1 (low M(r) activity 1) relocation, and cis-SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex disassembly; docking, mediated by Ypt7p and trans-SNARE association; and fusion of docked vacuoles. Ca(2+) and calmodulin regulate late stages of the reaction. We now show that the vacuole proton gradient, generated by the vacuolar proton ATPase, is needed for trans-SNARE complex formation during docking and hence for the subsequent LMA1 release. Though neither the vacuolar Pmc1p Ca(2+)-ATPase nor the Vcx1p Ca(2+)/H(+) exchanger are needed for the fusion reaction, they participate in Ca(2+) and Delta mu(H)(+) homeostasis. Fusion itself does not require the maintenance of trans-SNARE pairs.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder that involves motoneuron degeneration, paralysis, and death. Mutations in Cu, Zn superoxide dismutase (SOD1) are one cause of this disease. It has been a puzzle as to why mutations in SOD1, an enzyme expressed in many neuronal types, selectively kill motoneurons. To begin to explore the factors that determine this selectivity, we carried out peripheral axotomy in mice expressing a mutant SOD1 (G93A mice) and controls (nontransgenic mice and mice expressing wild-type human SOD1). Axotomy in controls induced a predicted axonal atrophy and a small degree of axon loss. The axonal atrophy led to an increase in the number of small axons and a decrease in the number of large axons. In contrast to the controls, axotomy in G93A mice reduced the extent of axon degeneration at the end stage of the disease, leading to an increase in the number of surviving motor axons. Interestingly, all of the increased surviving axons were in the axon group with diameters smaller than 4.5 microm. This result suggests an apparent threshold of vulnerability that is correlated with axon size.
gC1q-R, a multifunctional protein, was found to bind with the carboxyl-terminal cytoplasmic domain of the alpha(1B)-adrenergic receptor (173 amino acids, amino acids 344-516) in a yeast two-hybrid screen of a cDNA library prepared from the rat liver. In a series of studies with deletion mutants in this region, the ten arginine-rich amino acids (amino acids 369-378) were identified as the site of interaction. The interaction was confirmed by specific co-immunoprecipitation of gC1q-R with full-length alpha(1B)-adrenergic receptors expressed on transfected COS-7 cells, as well as by fluorescence confocal laser scanning microscopy, which showed co-localization of these proteins in intact cells. Interestingly, the alpha(1B)-adrenergic receptors were exclusively localized to the region of the plasma membrane in COS-7 cells that expressed the alpha(1B)-adrenergic receptor alone, whereas gC1q-R was localized in the cytoplasm in COS-7 cells that expressed gC1q-R alone; however, in cells that co-expressed alpha(1B)-adrenergic receptors and gC1q-R, most of the alpha(1B)-adrenergic receptors were co-localized with gC1q-R in the intracellular region, and a remarkable down-regulation of receptor expression was observed. These observations suggest a new role for the previously identified complement regulatory molecule, gC1q-R, in regulating the cellular localization and expression of the alpha(1B)-adrenergic receptors.
The interferon-induced double-stranded RNA-activated protein kinase PKR is the prototype of a class of double-stranded (dsRNA)-binding proteins (DRBPs) which share a dsRNA-binding motif conserved from Drosophila to humans. Here we report the purification of DRBP76, a new human member of this class of proteins. Sequence from the amino terminus of DRBP76 matched that of the M phase-specific protein, MPP4. DRBP76 was also cloned by the yeast two-hybrid screening of a cDNA library using a mutant PKR as bait. Analysis of the cDNA sequence revealed that it is the full-length version of MPP4, has a bipartite nuclear localization signal, two motifs that can mediate interactions with both dsRNA and PKR, five epitopes for potential M phase-specific phosphorylation, two potential sites for phosphorylation by cyclin-dependent kinases, a RG2 motif present in many RNA-binding proteins and predicts a protein of 76 kDa. DsRNA and PKR interactions of DRBP76 were confirmed by analysis of in vitro translated and purified native proteins. Cellular expression of an epitope-tagged DRBP76 demonstrated its nuclear localization, and its co-immunoprecipitation with PKR demonstrated that the two proteins interact in vivo. Finally, purified DRBP76 was shown to be a substrate of PKR in vitro, indicating that this protein's cellular activities may be regulated by PKR-mediated phosphorylation.