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H Xu

Publications and source records attributed to H Xu.

At least 559 records · Page 31Linked to original sources
PubMed1996

Transport of vesicular stomatitis virus G protein to the cell surface is signal mediated in polarized and nonpolarized cells.

Current model propose that in nonpolarized cells, transport of plasma membrane proteins to the surface occurs by default. In contrast, compelling evidence indicates that in polarized epithelial cells, plasma membrane proteins are sorted in the TGN into at least two vectorial routes to apical and basolateral surface domains. Since both apical and basolateral proteins are also normally expressed by both polarized and nonpolarized cells, we explored here whether recently described basolateral sorting signals in the cytoplasmic domain of basolateral proteins are recognized and used for post TGN transport by nonpolarized cells. To this end, we compared the inhibitory effect of basolateral signal peptides on the cytosol-stimulated release of two basolateral and one apical marker in semi-intact fibroblasts (3T3), pituitary (GH3), and epithelial (MDCK) cells. A basolateral signal peptide (VSVGp) corresponding to the 29-amino acid cytoplasmic tail of vesicular stomatitis virus G protein (VSVG) inhibited with identical potency the vesicular release of VSVG from the TGN of all three cell lines. On the other hand, the VSVG peptide did not inhibit the vesicular release of HA in MDCK cells not of two polypeptide hormones (growth hormone and prolactin) in GH3 cells, whereas in 3T3 cells (influenza) hemagglutinin was inhibited, albeit with a 3x lower potency than VSVG. The results support the existence of a basolateral-like, signal-mediated constitutive pathway from TGN to plasma membrane in all three cell types, and suggest that an apical-like pathway may be present in fibroblast. The data support cargo protein involvement, not bulk flow, in the formation of post-TGN vesicles and predict the involvement of distinct cytosolic factors in the assembly of apical and basolateral transport vesicles.

3T3 Cells↗
PubMed1996

Merosin and laminin in myogenesis; specific requirement for merosin in myotube stability and survival.

Laminin (laminin-1; alpha 1-beta 1-gamma 1) is known to promote myoblast proliferation, fusion, and myotube formation. Merosin (laminin-2 and -4; alpha 2-beta 1/beta 2-gamma 1) is the predominant laminin variant in skeletal muscle basement membranes; genetic defects affecting its structure or expression are the causes of some types of congenital muscular dystrophy. However, the precise nature of the functions of merosin in muscle remain unknown. We have developed an in vitro system that exploits human RD and mouse C2C12 myoblastic cell lines and their clonal variants to study the roles of merosin and laminin in myogenesis. In the parental cells, which fuse efficiently to multinucleated myotubes, merosin expression is upregulated as a function of differentiation while laminin expression is downregulated. Cells from fusion-deficient clones do not express either protein, but laminin or merosin added to the culture medium induced their fusion. Clonal variants which fuse, but form unstable myotubes, express laminin but not merosin. Exogenous merosin converted these myotubes to a stable phenotype, while laminin had no effect. Myotube instability was corrected most efficiently by transfection of the merosin-deficient cells with the merosin alpha 2 chain cDNA. Finally, merosin appears to promote myotube stability by preventing apoptosis. Hence, these studies identify novel biological functions for merosin in myoblast fusion and muscle cell survival; furthermore, these explain some of the pathogenic events observed in congenital muscular dystrophy caused by merosin deficiency and provide in vitro models to further investigate the molecular mechanisms of this disease.

Animals↗
PubMed1996

Developmental analysis reveals mismatches in the expression of K+ channel alpha subunits and voltage-gated K+ channel currents in rat ventricular myocytes.

In the experiments here, the developmental expression of the functional Ca(2+)-independent, depolarization-activated K+ channel currents, Ito and IK, and of the voltage-gated K+ channel (Kv) alpha subunits, Kv1.2, Kv1.4, Kv1.5, Kv2.1, and Kv4.2 in rat ventricular myocytes were examined quantitatively. Using the whole-cell patch clamp recording method, the properties and the densities of Ito and IK in ventricular myocytes isolated from postnatal day 5 (P5), 10 (P10), 15 (P15), 20 (P20), 25 (P25), 30 (P30), and adult (8-12 wk) rats were characterized and compared. These experiments revealed that mean Ito densities increase fourfold between birth and P30, whereas IK densities vary only slightly. Neither the time- nor the voltage-dependent properties of the currents vary measurably, suggesting that the subunits underlying functional Ito and IK channels are the same throughout postnatal development. In parallel experiments, the developmental expression of each of the voltage-gated K+ channel alpha subunits, Kv1.2, Kv1.4, Kv1.5, Kv2.1, and Kv4.2, was examined quantitatively at the mRNA and protein levels using subunit-specific probes. RNase protection assays revealed that Kv1.4 message levels are high at birth, increase between P0 and P10, and subsequently decrease to very low levels in adult rat ventricles. The decrease in message is accompanied by a marked reduction in Kv1.4 protein, consistent with our previous suggestion that Kv1.4 does not contribute to the formation of functional K+ channels in adult rat ventricular myocytes. In contrast to Kv1.4, the mRNA levels of Kv1.2, Kv1.5, Kv2.1, and Kv4.2 increase (three- to five-fold) between birth and adult. Western analyses, however, revealed that the expression patterns of these subunits proteins vary in distinct ways: Kv1.2 and Kv4.2, for example, increase between P5 and adult, whereas Kv1.5 remains constant and Kv2.1 decreases. Throughout development, therefore, there is a mismatch between the numbers of Kv alpha subunits expressed and the functional voltage-gated K+ channel currents distinguished electrophysiologically in rat ventricular myocytes. Alternative experimental approaches will be required to define directly the Kv alpha subunits that underlie functional voltage-gated K+ channels in these (and other) cells. In addition, the finding that Kv alpha subunit protein expression levels do not necessarily mirror mRNA levels suggests that caution should be exercised in attempting functional interpretations of observed changes in mRNA levels alone.

Age Factors↗
PubMed1996

Interferon-gamma inducible protein (IP-10) expression is mediated by CD8+ T cells and is regulated by CD4+ T cells during the elicitation of contact hypersensitivity.

To investigate the potential roles of CD4+ and CD8+ T cells during contact hypersensitivity, we examined the T-cell-dependent expression of proinflammatory cytokine genes in the responses to dinitrofluorobenzene and oxazolone. Whole cell RNA was isolated from challenged ear tissue and analyzed for level of cytokine gene expression by Northern blot and densitometry analysis. Expression of interleukin 1 beta and the three chemokine genes (IP-10, JE, and KC) examined was dependent on the hapten dose used for sensitization and correlated with the immune response, i.e., ear swelling, elicited. Antibody-mediated depletion of CD8+ T cells before sensitization resulted in the absence of IP-10 expression following hapten challenge, indicating the ability of immune CD8+ T cells to mediate IP-10 expression. Depletion of CD4+ T cells resulted in higher levels of IP-10 and KC expression during elicitation of contact sensitivity, suggesting CD4+ T cells inhibit the expression of these proinflammatory genes. Depletion of CD4+ T cells resulted in contact hypersensitivity responses of higher magnitude and depletion of CD8+ T cells resulted in responses of lower magnitude. Transfer of CD8+ T-cell-depleted immune cells resulted in low, but detectable levels of IP-10 expression, indicating the ability of some oxazolone-immune CD4+ T cells to mediate IP-10 expression. These results indicate the differential induction of proinflammatory cytokine gene expression during elicitation of contact hypersensitivity in which expression of IP-10 is primarily mediated by immune CD8+ T cells and inhibited by immune CD4+ T cells.

Animals↗
PubMed1996

2-Amino-4-methylpyridine as a potent inhibitor of inducible NO synthase activity in vitro and in vivo.

1. The ability of 2-amino-4-methylpyridine to inhibit the catalytic activity of the inducible NO synthase (NOS II) enzyme was characterized in vitro and in vivo. 2. In vitro, 2-amino-4-methylpyridine inhibited NOS II activity derived from mouse RAW 264.7 cells with an IC50 of 6 nM. Enzyme kinetic studies indicated that inhibition is competitive with respect to arginine. 2-Amino-4-methylpyridine was less potent on human recombinant NOS II (IC50 = 40 nM) and was still less potent on human recombinant NOS I and NOS III (IC50 = 100 nM). NG-monomethyl-L-arginine (L-NMMA), N6-iminoethyl-L-lysine (L-NIL) and aminoguanidine were much weaker inhibitors of murine NOS II than 2-amino-4-methylpyridine but, unlike 2-amino-4-methylpyridine, retained similar activity on human recombinant NOS II. L-NMMA inhibited all three NOS isoforms with similar potency (IC50S 3-7 microM). In contrast, compared to activity on human recombinant NOS III, L-NIL displayed 10 x selectivity for murine NOS II and 11 x selectivity for human recombinant NOS II while aminoguanidine displayed 7.3 x selectivity for murine NOS II and 3.7 x selectivity for human recombinant NOS II. 3. Mouse RAW 264.7 macrophages produced high levels of nitrite when cultured overnight in the presence of lipopolysaccharide (LPS) and interferon-gamma. Addition of 2-amino-4-methylpyridine at the same time as the LPS and IFN-gamma, dose-dependently reduced the levels of nitrite (IC50 = 1.5 microM) without affecting the induction of NOS II protein. Increasing the extracellular concentration of arginine decreased the potency of 2-amino-4-methylpyridine but at concentrations up to 10 microM, 2-amino-4-methylpyridine did not inhibit the uptake of [3H]-arginine into the cell. Addition of 2-amino-4-methylpyridine after the enzyme was induced also dose-dependently inhibited nitrite production. Together, these data suggest that 2-amino-4-methylpyridine reduces cellular production of NO by competitive inhibition of the catalytic activity of NOS II, in agreement with results obtained from in vitro enzyme kinetic studies. 4. When infused i.v. in conscious unrestrained rats, 2-amino-4-methylpyridine inhibited the rise in plasma nitrate produced in response to intraperitoneal injection of LPS (ID50 = 0.009 mg kg-1 min-1). Larger doses of 2-amino-4-methylpyridine were required to raise mean arterial pressure in untreated conscious rats (ED50 = 0.060 mg kg-1 min-1) indicating 6.9 x selectivity for NOS II over NOS III in vivo. Under the same conditions, L-NMMA was nonselective while L-NIL and aminoguanidine displayed 5.2 x and 8.6 x selectivity respectively. All of these compounds caused significant increases in mean arterial pressure at doses above the ID50 for inhibition of NOS II activity in vivo. 5. 2-Amino-4-methylpyridine also inhibited LPS-induced elevation in plasma nitrate after either subcutaneous (ID50 = 0.3 mg kg-1) or oral (ID50 = 20.8 mg kg-1) administration. 6. These data indicate that 2-amino-4-methylpyridine is a potent inhibitor of NOS II activity in vitro and in vivo with a similar degree of isozyme selectivity to that of L-NIL and aminoguanidine in rodents.

Animals↗
PubMed1996

Characterization of a stimulatory adenosine A2a receptor in adult rat ventricular myocyte.

The expression and function of stimulatory adenosine A2 receptor on the cardiac myocyte is not well defined. The objective of the present study is to characterize the A2a receptor in adult rat cardiac ventricular myocytes. After selection of an optimal lot of collagenase for myocyte isolation and for consistent measurement of adenosine-mediated responses, the A1-receptor pathway was inactivated by pertussis toxin and by the A1-selective antagonist 1,3-dipropyl-8-cyclopentylxanthine. Effects of the adenosine agonist and antagonist or cardiac myocyte contractile amplitude and on adenosine 3',5'-cyclic monophosphate (cAMP) levels were determined. The A2a-receptor-selective agonist 2-[p-(2-carboxyethyl)phenylethylamino]-5'-N-ethylcarboxamidoade nos ine (CGS-21680) caused a pronounced stimulation of myocyte contractile amplitude and an increase in the cAMP level, as did the nonselective agonists 5'-(N-ethylcarboxamido) adenosine (NECA) and adenosine. The A2a-receptor-selective antagonist 8-(3-chlorostyryl)caffeine blocked the NECA- and adenosine-induced positive inotropic response. Probing of myocyte RNA with a rat A2a-receptor cDNA demonstrated a 2.6-kb mRNA, corresponding to that encoding the A2a receptor. Together, data from contractile, cAMP, and RNA studies indicate that A2a receptors are expressed and are functionally coupled to stimulation of cAMP accumulation and cardiac contractility in adult rat ventricular myocytes.

Adenosine↗
PubMed1996

Historical development of Chinese dietary patterns and nutrition from the ancient to the modern society.

Actually, food, diet and diet therapy germinated together with the change of meal patterns and traditional Chinese medicine from very ancient China; they appeared in an embryonic form till the Shang and Zhou Dynasties and received great importance from the governors who arranged officials to manage their diets and banquets. Moreover, food, diet and meal patterns were replenished through the Zhou, Qin, Han and Jin Dynasties and epitomized and reached thriving and prosperous standards till the Tang Dynasty. They then became perfected, developed, and formed a complete theory in the dynasties of Song, Jin, Yuan, Ming and Qing. The basis of modern nutrition was made up until the end of 19th century and the beginning of 20th century, which was the time when natural science, including microbiology, chemistry, food industry, etc. were extended into China, yet it was not fully formed until the established of the People's Republic of China. Practicing, teaching, training and research activities started regularly in 1950. With a big population and poor economy basis, the first problem that the Chinese people has now been basically solved. Chinese nutritional scientists worked hard to find out the nutritional problems and status of the people. Through the broad-scale 'Nationwide Nutrition Survey', we now understand our main problems. On this basis, RDA, dietary goal and dietary guidance have been put forward. Although the problem of adequate food and clothing has been basically solved, the Chinese are still facing both the problem of nutrition insufficiency and nutrition excess. However, although nutrition insufficiency and deficiency still extensively exist, nutrition excess and imbalance are emerging in other sections of the population. There is still a shortage of qualified nutritional scientists and technicians, and the training of nutritionists is urgent. Food supplies, including milk, beef, green vegetables and fruit should be increased, especially for some rural and remote areas. The good traditional eating habits and meal patterns should be kept, e.g., breakfast and lunch cannot be neglected, and plant protein meals and Chinese medicinal diets should be promoted. Animals fat intake and fried foods should be reduced, and exercise and fitness programs should be recommended for the overweight population. In the future, our meal pattern take on a mixed form with the advantages of both the eastern and western diets. Chinese scientists are confident of solving the nutritional problems and improving the whole nation's physical fitness and physique under the situation of gradual improvements of the economy and nutritional status of people.

Aged↗
PubMed1996

CSF-1 deficiency in mice results in abnormal brain development.

Colony stimulating factor-1 (CSF-1) was initially identified as a growth factor for mononuclear phagocytes. This study examines the role of CSF-1 in the development of the central nervous system (CNS). CSF-1 treatment of neurons cultured from embryonic brain promoted survival and process outgrowth in a dose-dependent manner. By contrast, CSF-1 treatment of neurons cultured from the osteopetrotic (op/op) mouse, a null mutant for CSF-1, promoted significantly less process outgrowth, suggesting that there are neural abnormalities in op/op animals. Nuclease protection assays were used to determine whether CSF-1 and its receptor are expressed at times appropriate to regulate neural development. Both CSF-1 and its receptor are expressed in developing mouse brain, with a unique pattern of CSF-1 mRNA splice variant expression encoding secreted, and not membrane-bound, growth factor. To determine whether brain function is altered by null mutation of CSF-1, op/op mice were examined using electrophysiologic assays. Brainstem auditory and visual evoked potentials were both abnormal in op/op mice. Further, intracortical recordings revealed aberrant neuronal function within visual cortex and alterations in the cortical circuitry that balances excitation and inhibition. Daily CSF-1 injection of postnatal op/op mice largely rescued the abnormal neural phenotype, confirming that the absence of CSF-1 during development is responsible for the abnormalities. The effects of CSF-1 on cultured embryonic neural cells, the developmentally appropriate expression of CSF-1 and its receptor, and the neurological abnormalities in op/op mice suggest a role for CSF-1 in brain development.

Animals↗
PubMed1996

Linoleate impairs collagen synthesis in primary cultures of avian chondrocytes.

The effects of supplemental fatty acids, vitamin E (VIT E), and iron-induced oxidative stress on collagen synthesis, cellular injury, and lipid peroxidation were evaluated in primary cultures of avian epiphyseal chondrocytes. The treatments included oleic and linoleic acids (O or 50 microM) complexed with BSA and dl-alpha-tocopheryl acetate (VIT E at 0 or 100 microM). After 14 days of preculture, the chondrocytes were enriched with fatty acids for 8 days then cultured with VIT E for 2 days. The chondrocytes were then treated with ferrous sulfate (O or 20 microM) for 24 hr to induce oxidative stress. Collagen synthesis was the lowest and the activity of lactate dehydrogenase (LDH) was the highest in chondrocyte cultures treated with 50 microM linoleic acid and 0 VIT E. In contrast, VIT E supplemented at 100 microM partially restored collagen synthesis in the chondrocytes enriched with linoleic acid and lowered LDH activity in the media. The iron oxidative inducer significantly increased the values of thiobarbituric acid-reactive substances (TBARS) in the culture medium. The data showed that linoleic acid impaired chondrocyte cell function and caused cellular injury but that VIT E reversed these effects. Results from a previous study demonstrated that VIT E stimulated bone formation in chicks fed unsaturated fat, and the present findings in cultures of epiphyseal chondrocytes suggest that VIT E is important for chondrocyte function in the presence of polyunsaturated fatty acids. VIT E appears to be beneficial for growth cartilage biology and in optimizing bone growth.

Animals↗
PubMed1996

[Quality of semen Hydnocarpi anthelminiticae introduced to various places].

The result shows that the Semen Hydnocarpi Anthelminticae introduced in Guangdong, Hainan and Yunnan Provinces is similar to the control medicinal materials in fatty oil content, index of refraction, effective component content and trace element content. But the saponification value of the introduced products is higher. The quality of the Semen Hydnocarpi Anthelminticae introduced to the above places is up to the level of the control medicinal materials.

China↗
PubMed1996

[Establishment of cervical lymph node metastasis in model rats and its microcirculation characteristics].

To determine the effects of vasoactive agents on blood flow in lymph node metastases, the blood flow in the cervical lymph node metastases and normal tissue were meassured using a hydrogen clearance method, at normotensive state, angiotensin I (A I) induced hypertensive state and sodium nitroprusside (SNP) induced hypotensive state. The metastases occurred frequently in the cervical lymph nodes of 17 rats on day 11-14 after Yoshida ascites hepatoma. AH109A cells were subcutaneously inoculated into back of auricule of 20 rats. The blood flow in the liver, brain and bone marrow of normal rats was of no significant changes when the mean arterial blood pressure (MABP) was elevated to approximately 20 kPa by infusion of A I and decreased to approximately 9.06 kPa by infusion of SNP. But the blood flow in the metastatic lymph nodes was increased from 1.42 +/- 0.48 ml.kg-1/s to 3.45 +/- 1.33 ml.kg-1/s (n = 13, P < 0.05) when the MABP was elevated from 14.81 +/- 1.04 kPa to 18.93 +/- 0.92 kPa by A I. On the contrary, the blood flow in the metastatic lymph node was decreased to 0.55 +/- 0.25 ml.kg-1/s (n = 13, P < 0.05) when the MABP was decreased to 8.84 +/- 0.63 kPa by SNP. The results indicated that microcirculation characteristics in the cervical lymph node metastases were different from those in the normal tissues. A I induced hypertension was useful to selectively improve delivery of chemotherapeutic drugs to the site of metastases. On the other hand, SNP induced hypotension may be useful to suppress washout of the drugs.

Animals↗
PubMed1996

[Observation of proliferative capacity of rat salivary gland cells].

Proliferative potentiality of adult rat salivary gland cells was studied by means of bromodeoxyuridine (BrdU) labeling in different time and ABC immunohistochemistry. The labeling rate of intercalated cells in different time after BrdU injection manifest the character of stem cell which is concordant with the theory of semipluripotential bicellular reserve cell suggested by Eversole and Batsakis. This initial labeling rate of intercalated cell is very low and it rises very rapidly to 78 times within 5 days. On the other hand, it also goes down very fast. We proved that the acinar cells and striated cells have the capacity of proliferation which is not so high as intercalated cells for self renewal that can complete the theory of semipluripotential bicellular reserve cell and is beneficial to explain why there is a variety of salivary gland neoplasms.

Animals↗
PubMed1996

[Effect of interferon-gamma on antigen-induced eosinophil infiltration in mouse airway].

Repeated aerosolized ovalbumin (OVA) challenge of OVA-sensitized mice induces bronchoalveolar lavage fluid (BALF) eosinophilia. The influence of interferon-gamma (IFN-gamma) on antigen-induced eosinophil recruitment in the airway as well as the concentration of interleukin-5 (IL-5) in supernatants of cultured spleen cells were examined. In sensitized mice challenged with OVA 20 minutes once a day for 6 days, the number of BALF eosinophils was (9.53 +/- 0.84) x 10(8)/L. However, no eosinophil could be found in the BALF from mice without OVA sensitization and challenge. In mice treated with intraperitoneal injection of INF-gamma before each challenge, different doses of IFN-gamma (1.0 x 10(3) U/kg, 1.0 x 10(4) U/kg and 1.0 x 10(5) U/kg) produced different degrees of eosinophilia inhibition 29.8% (P < 0.05), 55.7% (P < 0.01) and 69.0% (P < 0.01). Our results showed that IFN-gamma prevented antigen-induced eosinophil infiltration in airway accompanied by a decrement of levels of IL-5 with a dose related response. It is concluded that IFN-gamma is capable of inhibiting eosinophil infiltration in mouse airway by inhibiting the production of IL-5. Our results suggested that IFN-gamma may be of value in eliminating asthmatic airway inflammation in humans.

Animals↗