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Biomedical subjects

Y Guo

Publications and source records attributed to Y Guo.

At least 433 records · Page 24Linked to original sources
PubMed1997

Effects of lipid headgroup and packing stress on poly(ethylene glycol)-induced phospholipid vesicle aggregation and fusion.

The effect of lipid headgroup and curvature-related acyl packing stress on PEG-induced phospholipid vesicle aggregation and fusion were studied by measuring vesicle and aggregate sizes using the quasi-elastic light scattering and fluorescence energy transfer techniques. The effect of the lipid headgroup was monitored by varying the relative phosphatidylcholine (PC) and phosphatidylethanolamine (PE) contents in the vesicles, and the influence of hydrocarbon chain packing stress was controlled either by the relative amount of PE and PC content in the vesicles, or by the degree of unsaturation of the acyl chains of a series of PEs, e.g., dilinoleoylphosphatidylethanolamine (dilin-PE), lysophosphatidylethanolamine (lyso-PE), and transacylated egg phosphatidylethanolamine (TPE). The PEG threshold for aggregation depends only weakly on the headgroup composition of vesicles. However, in addition to the lipid headgroup, the curvature stress of the monolayer that forms the vesicle walls plays a very important role in fusion. Highly stressed vesicles, i.e., vesicles containing PE with highly unsaturated chains, need less PEG to induce fusion. This finding applies to the fusion of both small unilamellar vesicles and large unilamellar vesicles. The effect of electrostatic charge on vesicle aggregation and fusion were studied by changing the pH of the vesicle suspension media. At pH 9, when PE headgroups are weakly charged, increasing electrostatic repulsion between headgroups on the same bilayer surface reduces curvature stress, whereas increasing electrostatic repulsion between apposing bilayer headgroups hinders intervesicle approach, both of which inhibit aggregation and fusion, as expected.

Acylation↗
PubMed1997

Translocation t(7;11)(P15;P15) in a patient with therapy-related acute myeloid leukemia following bimolane and ICRF-154 treatment for psoriasis.

The t(7;11)(p15;p15) translocation is an uncommon balanced aberration which has been found predominantly in Orientals, frequently presenting as de novo acute myeloid leukemia (AML) and occasionally as chronic myeloid leukemia in blastic crisis. This paper reports the first case of therapy-related AML (t-AML) with t(7;11). The patient was a 36-year-old Chinese man with a longstanding psoriasis for which he had received bimolane and ICRF-154 therapy. His cytology and cytochemistry were compatible with M2 subtype of AML. He achieved a complete remission after two courses of HA regimen (homoharringtonine and Ara-c). Six months later, he relapsed and died of overwhelming infection after 3 months. Chromosome analysis on bone marrow cells using short-term culture and R-banding at presentation revealed his karyotype to be 46,XY,t(7;11)(p15;p15)/ 46,XY,t(7;11)(p15;p15),del(12)(p12)/ 46,XY. This case implies: (1) dioxopiperazine derivatives can induce AML with t(7;11) in addition to inducing AML with t(15;17) or t(8;21); (2) t(7;11) may be found not only in de novo AML, but also in t-AML. Chromosomal translocation t(7;11) should be added to t(8;21), t(15;17) and inv(16) as favourable cytogenetic abnormalities associated with t-AML.

Acute Disease↗
PubMed1997

Fast numerical algorithms for fitting multiresolution hybrid shape models to brain MRI.

In this paper, we present new and fast numerical algorithms for shape recovery from brain MRI using multiresolution hybrid shape models. In this modeling framework, shapes are represented by a core rigid shape characterized by a superquadric function and a superimposed displacement function which is characterized by a membrane spline discretized using the finite-element method. Fitting the model to brain MRI data is cast as an energy minimization problem which is solved numerically. We present three new computational methods for model fitting to data. These methods involve novel mathematical derivations that lead to efficient numerical solutions of the model fitting problem. The first method involves using the nonlinear conjugate gradient technique with a diagonal Hessian preconditioner. The second method involves the nonlinear conjugate gradient in the outer loop for solving global parameters of the model and a preconditioned conjugate gradient scheme for solving the local parameters of the model. The third method involves the nonlinear conjugate gradient in the outer loop for solving the global parameters and a combination of the Schur complement formula and the alternating direction-implicit method for solving the local parameters of the model. We demonstrate the efficiency of our model fitting methods via experiments on several MR brain scans.

Algorithms↗
PubMed1997

t(8;20)(q22;p13): a novel variant translocation of t(8;21) in acute myeloblastic leukaemia.

A novel variant translocation t(8;20)(q22;p13) detected by karyotype analysis of bone marrow cells using R- and G-banding techniques, is reported in a case of M2-acute myeloid leukaemia (AML). The leukaemic cells were indistinguishable morphologically from that of M2-AML with t(8;21)translocation. RT-PCR revealed no AML1/ETO fusion transcript, but the wild-type ETO-3' was expressed in the bone marrow cells suggesting that t(8;20) is a true simple variant translocation of t(8;21), and that a fusion gene consisting of ETO and an unidentified gene located in band 20p13 may exist in our case. Further study is required to clarify the entity of the assumed fusion gene.

Aged↗
PubMed1997

Intranasal immunization of mice with PspA (pneumococcal surface protein A) can prevent intranasal carriage, pulmonary infection, and sepsis with Streptococcus pneumoniae.

Many pathogens, including Streptococcus pneumoniae, are carried asymptomatically on the nasopharyngeal mucosa and spread among individuals by close contact. Clinical disease results when pneumococci escape from the mucosa and invade sterile sites. Although systemic immunity can prevent invasive disease, control of person-to-person spread is probably dependent on immunity acting at the mucosal surface. Intranasal immunization of mice with PspA (pneumococcal surface protein A) or a capsular 6B polysaccharide-tetanus toxoid conjugate induced mucosal and systemic antibody responses and provided long-lasting protection against carriage of S. pneumoniae. Resistance to carriage was dependent on mucosal rather than systemic immunity and was effective against heterologous strains of heterologous PspA types. Intranasal immunization with PspA also protected against systemic infection following intravenous, intratracheal, and intraperitoneal challenge.

Animals↗
PubMed1997

Molecular cloning and gene expression analysis of PSP94 (prostate secretory protein of 94 amino acids) in primates.

Prostate secretory protein of 94 amino acids (PSP94) has shown the potential to be a diagnostic biomarker and a therapeutic agent for prostate cancer. Primates have been the main animal models for studying the biology of this molecule. We have cloned and analyzed the cDNA and promoter region of PSP94 from baboon (Papio anubis). Sequence divergence among baboon, monkey, pig, and human, in both the exons and 5'-flanking region indicates rapid evolution of the PSP94 gene. There are conserved steroid hormone response elements (SHRE) in the promoter region of all three primate species. Multiple, alternative transcripts starting near these SHREs and upstream to the TATA box were identified by reverse transcriptase polymerase chain reaction (RT-PCR) and rapid amplification of 5'-cDNA ends (5' RACE) in primate prostatic tissues. This differential transcription initiation may be linked to androgen regulation of PSP94 gene expression. PSP94 transcripts were detected by RT-PCR in a wide variety of mucus-secreting tissues. However, the alternative transcripts were found only in the prostate. The distribution of the PSP94 protein in baboon secretory tissues was also examined by Western blot analysis using a polyclonal antibody against the human homolog. A positive immunoreactive band was detected, but it was weak, due probably to epitope divergence between the two species. In all young, healthy primate animals tested, the level of immunoreactive PSP94 in prostate tissues was lower than expected. In addition, RT-PCR combined with Southern blot analysis on prostate tissues in these animals failed to detect the PSP57 mRNA produced by alternative splicing of PSP94 primary transcript. These observations can be explained by the sexual immaturity and incomplete prostate development in these young primates. This explanation was supported by histological examination of their prostate during PSP94 immunohistochemistry.

Amino Acid Sequence↗
PubMed1997

DNA-binding determinants of sigma 54 as deduced from libraries of mutations.

PCR mutagenesis was used to obtain libraries of mutations in the region between amino acids 300 and 400 in the DNA-binding domain of Escherichia coli sigma 54. Two hundred changes that did not alter function were identified. These were compared with a somewhat smaller number of changes that did alter function. Several important regions were identified. Single point mutations in two of these, near amino acids 363 and 383, destroyed the ability of sigma to bind DNA, as assayed by band shift analysis. A third segment from amino acids 327 to 347 is also a candidate for contributing to DNA binding. Comparison with data in the literature leads to testable proposals for the complex mode of DNA binding that is associated with sigma 54.

Amino Acid Sequence↗
PubMed1997

Protein kinase A phosphorylation and G protein regulation of type II pneumocyte Na+ channels in lipid bilayers.

Protein kinase A (PKA)- and G protein-mediated regulation of immunopurified adult rabbit alveolar epithelial type II (ATII) cell proteins that exhibit amiloride-sensitive Na+ channel activity was studied in planar lipid bilayers and freshly isolated ATII cells. Addition of the catalytic subunit of PKA + ATP increased single channel open probability from 0.42 +/- 0.05 to 0.82 +/- 0.07 in a voltage-independent manner, without affecting unitary conductance. This increase in open probability of the channels was mainly due to a decrease in the time spent by the channel in its closed state. The apparent inhibition constant for amiloride increased from 8.0 +/- 1.8 microM under control conditions to 15 +/- 3 microM after PKA-induced phosphorylation; that for ethylisopropylamiloride increased from 1.0 +/- 0.4 to 2.0 +/- 0.5 microM. Neither pertussis toxin (PTX) nor guanosine 5'-O-(3-thiotriphosphate) affected ATII Na+ channel activity in bilayers. Moreover, PTX failed to affect amiloride-inhibitable 22Na+ uptake in freshly isolated ATII cells. In vitro, ADP ribosylation induced by PTX revealed the presence of a specifically ribosylated band at 40-45 kDa in the total solubilized ATII cell protein fraction, but not in the immunopurified fraction. Moreover, the immunopurified channel was downregulated in response to guanosine 5'-O-(3-thiotriphosphate)-mediated activation of the exogenous G alpha(i-2), but not G(oA), G alpha(i-1), or G alpha(i-3), protein added to the channel. This effect occurred only in the presence of actin. These results suggest that amiloride-sensitive Na+ channels in adult alveolar epithelia regulated by PKA-mediated phosphorylation also retain the ability to be regulated by G alpha([i-2), but not G alpha([i-1) or G alpha(i-3), protein.

Amiloride↗
PubMed1997

Exosurf enhances adenovirus-mediated gene transfer to alveolar type II cells.

We assessed the role of surfactant replacement mixtures in the enhancement of adenovirus-mediated gene transfer to pulmonary epithelial cells both in vitro and in vivo. A549 cells, a pulmonary epithelium-derived adenocarcinoma cell line, were incubated with either media alone or media containing 10 microg phospholipid/ml Exosurf or Infasurf for 50 min followed by addition of a replication-deficient adenovirus (E1-deleted) expressing the luciferase reporter gene [AdCMV-Luc; 10 plaque-forming units (PFU)/cell] for 4 h. Pretreatment with Exosurf, but not Infasurf, at 37 degrees C, but not at 4 degrees C, enhanced luciferase activity in A549 cells 24 h later by 156% (P < 0.01). Intratracheal instillation of AdCMV-Luc (2 x 10(9) PFU) into rats resulted in luciferase expression mainly in alveolar macrophages and to a smaller extent in alveolar type II (ATII) cells 24 h later. However, when the AdCMV-Luc instillation was preceded by Exosurf (250 microl; 25 mg/ml), a 10-fold increase in ATII cell luciferase activity was noted. Preincubation of cultured ATII cells with Exosurf also enhanced their transfection by AdCMV-Luc by 515% (P < 0.001). The results of these studies provide a new strategy for targeting ATII cells for gene delivery.

Adenocarcinoma↗
PubMed1997

Hypercholesterolemia impairs a detoxification mechanism against peroxynitrite and renders the vascular tissue more susceptible to oxidative injury.

Previous studies have shown that glutathione (GSH) plays a central role in the protection against peroxynitrite (ONOO-) toxicity. The present study evaluated the changes of the GSH cytoprotective system against ONOO- in hypercholesterolemia and determined the effects of carvedilol, a beta-blocker with free radical-scavenging activity, on these hypercholesterol-induced changes. New Zealand White rabbits were fed either a normal diet, a high-cholesterol diet, or a high-cholesterol diet supplemented with either carvedilol or propranolol. Eight weeks later, the rabbits were killed, and the thoracic aortas were isolated. Total GSH content of aortic tissue, vasorelaxation response of aortic rings to exogenous ONOO-, No regeneration from ONOO- by aortic homogenate, and ONOO(-)-induced aortic tissue injury were examined. Hypercholesterolemia decreased tissue GSH content (0.52 +/- 0.08 versus 0.86 +/- 0.04 mumol/g in control, P < .01), attenuated the vasorelaxation response to ONOO- (40 +/- 4.1% versus 76 +/- 3.2%, P < .01), reduced NO regeneration from ONOO- (387 +/- 40 versus 662 +/- 51 pmol, P < .01), and potentiated ONOO(-)-induced vascular tissue injury (37 +/- 4.4% versus 14 +/- 2.6% of increase in lactate dehydrogenase release after 3-morpholinosydnonimine exposure, P < .01). Treatment of the hypercholesterolemic rabbits with carvedilol, but not propranolol, significantly preserved tissue GSH content (0.79 +/- 0.05 mumol/g, P < .01 versus nontreated hypercholesterolemic rabbits), restored the vasorelaxation to ONOO- (61 +/- 2%, P < .01), increased NO regeneration from ONOO- (583 +/- 39 pmol, P < .01), and attenuated ONOO(-)-induced tissue injury (19 +/- 1.8%, P < .01). These results suggest that hypercholesterolemia impairs the GSH-mediated detoxification mechanism against ONOO- and renders the vascular tissue more susceptible to oxidative injury. Carvedilol, a novel vasodilating beta-blocker with antioxidant activity, significantly preserved this self-defense system and protected tissue from oxidant injury.

Animals↗
PubMed1997

Evidence that late preconditioning against myocardial stunning in conscious rabbits is triggered by the generation of nitric oxide.

Recent studies in conscious pigs and rabbits have demonstrated that a series of brief coronary occlusions renders the heart relatively resistant to myocardial "stunning" 24 hours later (late preconditioning [PC] against stunning). The mechanism of this powerful cardioprotective response is unknown. The goal of the present study was to test the hypothesis that the development of late PC against stunning is triggered by increased generation of NO during the first ischemic challenge. Conscious rabbits underwent a sequence of six 4-minute coronary occlusion/4-minute reperfusion cycles for 3 consecutive days (days 1, 2, and 3). On day 1, rabbits received either an intravenous infusion of the NO synthase inhibitor NG-nitro-L-arginine (L-NA, 13 mg/kg before the first occlusion) (group II, n = 10) or vehicle (group I [control], n = 10). In the control group, on day 1 systolic wall thickening (WTh) in the ischemic/reperfused region remained significantly depressed for 4 hours after the sixth reperfusion, indicating myocardial stunning. On days 2 and 3, however, the recovery of WTh improved markedly, so that the total deficit of WTh decreased by 60% on day 2 and 55% on day 3 compared with day 1 (P < .01). In the L-NA-treated group, the total deficit of WTh on day 1 was similar to that observed in the control group. On day 2, however, the total deficit of WTh was not significantly different from that observed on day 1 and was 132% greater than that observed in control rabbits on day 2 (P < .01). On day 3, the total deficit of WTh was 66% less than that noted on day 2 (P < .01). Thus, in L-NA-treated rabbits the sequence of six coronary occlusions and reperfusions performed on day 1 failed to precondition against stunning on day 2, but the same sequence performed on day 2 did precondition against stunning on day 3. Another group of rabbits (group III, n = 6) received L-NA on day 1 in the absence of ischemia and was subjected to the occlusion/ reperfusion sequence on days 2 and 3. In these animals, the total deficit of WTh on day 2 did not differ from that observed in control rabbits on day 1, indicating that administration of L-NA did not exacerbate the severity of myocardial stunning 24 hours later; therefore, the absence of late PC against stunning on day 2 in group II cannot be ascribed to a delayed deleterious action of L-NA on WTh. In conclusion, these results demonstrate that the NO synthase inhibitor L-NA completely blocks the development of late PC against myocardial stunning in conscious rabbits, indicating that NO generated as a result of the PC ischemia triggers the development of the cardioprotective response observed 24 hours later. NO is known to exert numerous biological actions resulting in rapid but transient physiological responses. The present observations support a novel pathophysiological paradigm in which NO also plays a key role in the delayed myocardial adaptations to ischemic stress, acting as a signaling step in the transduction pathway that leads to increased resistance to subsequent ischemic injury.

Animals↗
PubMed1997

The protective effect of late preconditioning against myocardial stunning in conscious rabbits is mediated by nitric oxide synthase. Evidence that nitric oxide acts both as a trigger and as a mediator of the late phase of ischemic preconditioning.

Seventy-four conscious rabbits undergoing a sequence of six 4-minute coronary occlusion/4-minute reperfusion cycles for 3 consecutive days (days 1, 2, and 3) were assigned to nine groups. In group I (controls, n = 8), the recovery of systolic wall thickening (WTh) after the sixth reperfusion was markedly improved on days 2 and 3 compared with day 1, indicating late preconditioning (PC) against myocardial stunning; the total deficit of WTh after the sixth reperfusion was reduced by 56% on day 2 and 50% on day 3 compared with day 1 (P < .01). Administration on day 2 of the nonselective NO synthase (NOS) inhibitor N omega-nitro-L-arginine (L-NA) (group II, n = 8) or of the selective inducible NOS inhibitors aminoguanidine (AG) (group IV, n = 8) and S-methylisothiourea sulfate (SMT) (group VI, n = 6) completely abrogated late PC against stunning on day 2. On day 3, the expected PC effect became manifest in all groups. Administration of L-NA, AG, or SMT on day 1 (groups III [n = 7], V [n = 6], and VII [n = 5], respectively) had no discernible effect on the deficit of WTh on day 1, indicating that these agents do not augment the severity of myocardial stunning in nonpreconditioned myocardium. In group VIII (n = 7), the abrogation of late PC by SMT on day 2 was completely reversed by the concomitant administration of L-arginine (595 mg/kg IV), indicating that it was not due to nonspecific NOS-unrelated actions. Administration of L-arginine alone on day 2 (group IX [n = 5]) had no effect on the deficit of WTh. Furthermore, administration of L-NA on day 1 (group III) prevented the appearance of the PC effect on day 2, whereas AG (group V) and SMT (group VI) did not, suggesting that the development of late PC on day 1 is triggered by the endothelial (type III) isoform of NOS. This study demonstrates that three structurally different NOS inhibitors (L-NA, AG, and SMT), given 24 hours after the PC ischemia, consistently abrogate late PC against myocardial stunning in conscious rabbits, indicating that this cardioprotective effect is mediated by the activity of NOS. The results obtained with AG and SMT specifically implicate the inducible (type II) isoform as the mediator of the protection on day 2. Previous studies have shown that NO triggers the development of late PC. The present results indicate that NO plays a dual role in late PC against stunning, acting initially as the trigger and subsequently as the mediator of the protection.

Animals↗
PubMed1997

Expression of nitric oxide synthases and GTP cyclohydrolase I in the ventilatory and limb muscles during endotoxemia.

Nitric oxide synthases (NOS) convert L-arginine to nitric oxide in the presence of tetrahydrobiopterin (BH4). Two constitutive isoforms of NOS exist in normal skeletal muscle fibers, however, the existence of a third, the inducible isoform (iNOS), has never been detected in these fibers in vivo. Therefore, we assessed the influence of in vivo endotoxemia on skeletal muscle expression of constitutive and inducible NOS isoforms and GTP cyclohydrolase I, the rate limiting enzyme of BH4 synthesis. Two groups of rats were infused i.p. either with E. coli endotoxin (20 mg/kg, LPS group) or saline (saline group). Animals were killed 6 h later and the ventilatory and limb muscles were quickly frozen. Endotoxin infusion elicited a significant rise in NOS activity of the diaphragm, intercostal, soleus and gastrocnemius muscles. Reverse transcription-polymerase chain reaction (RT-PCR) on muscle total RNA detected very low expression of iNOS and GTP cyclohydrolase I mRNA in the saline group, but significant upregulation of both enzymes was found in the ventilatory and limb muscles of the LPS group. Immunoblotting detected no iNOS protein in the saline group but a significant iNOS protein expression was found in the diaphragm, intercostal and soleus muscles and to a lesser extent, in the gastrocnemius of the LPS group. Endotoxemia was also associated with increased protein expression of constitutive NOS isoforms mainly in the diaphragm and to lesser extent in the intercostal, gastrocnemius and soleus muscles. We conclude that in vivo exposure to endotoxin leads to differential induction of both iNOS and GTP cyclohydrolase I in the ventilatory and limb muscles.

Animals↗
PubMed1997

Molecular genetic analysis of V-ATPase function in Drosophila melanogaster.

V-ATPases are phylogenetically widespread, highly conserved, multisubunit proton pumps. Originally characterised in endomembranes, they have been found to energise transport across plasma membranes in a range of animal cells and particularly in certain epithelia. While yeast is the model of choice for the rapid generation and identification of V-ATPase mutants, it does not allow their analysis in a plasma membrane context. For such purposes, Drosophila melanogaster is a uniquely suitable model. Accordingly, we have cloned and characterised genes encoding several V-ATPase subunits in D. melanogaster and, using P-element technology, we have succeeded in generating multiple new alleles. Reporter gene constructs reveal ubiquitous expression, but at particularly high levels in those epithelial thought to be energised by V-ATPases, and several of the alleles have lethal recessive phenotypes characterised by epithelial dysfunction. These results, while providing the first gene knockouts of V-ATPases in animals, also illustrate the general utility of D. melanogaster as a model for the genetic analysis of ion transport and its control in epithelia.

Alleles↗
PubMed1997

[Epidemic trend of tuberculous meningitis in children of Heilongjiang province].

OBJECTIVE: To investigate the epidemic trend of tuberculous meningitis in children of Heilongjiang province in recent ten years, and to provide scientific evidence for control of the disease. METHODS: The data, registered by 82 counties' antituberculosis institute, of tuberculous meningitis patients under 14 years were analyzed, and the epidemic trend of the disease was also discussed. RESULTS: The incidence of tuberculous meningitis was 9.58 per 10,0000 populations in 1982, 2.17 per 10,0000 populations in 1992. The rate of annual decrease was 13.8%. CONCLUSION: Participation of the government, improvement of pelple's life standard, control of sources of infection, and vaccination of BCG are effective measures for decreasing the incidence of this disease.

Adolescent↗
PubMed1997

[Effects of different components of serum from radiation, burn and combined radiation-burn injury on L-type calcium channel of cultured myocardial cells].

The effects of different components of serum from radiation, burn and combined radiation-burn injury on the activity of L-type calcium channel in cultured myocardial cells were investigated in this study. The results revealed that the serum from different injury groups could all activate the L-type calcium channel of cultured myocardial cells. These changes altered the calcium level in cells, which might be an important cause of dysfunction in cardiovascular system. Among the components of postinjury serum, the effect of high molecular components (> 8-10 kD) was not significant, whereas low molecule (< 8-10kD) and lipid components were the major effective components. The low molecule of postinjury serum affected not only on the opening activity of L-type channel, but also on the state of molecular movement in the membrane. The effect of serum lipids from injury groups could be depressed by SOD, which suggests that there may be free radical reactions during the serum lipids effect on calcium channel. The effects of serum and its components from combined radiation-burn group were the most intensive, and those from radiation injury were the weakest. The nature of the toxic material in serum remains to be further investigated.

Animals↗
PubMed1997

[Epidemiologic study of diabetic retinopathy in Capital Steel Company].

OBJECTIVE: To investigate the prevalence and risk factors of diabetic retinopathy. METHOD: 29,938 subjects aged 30 years or older were screened for diabetic retinopathy in Capital Steel Company. RESULTS: Among the 955 subjects (3.19%) proved to have diabetes mellitus, 534 subjects underwent ophthalmoscopic and fluorescein angiographic examinations. Diabetic retinopathy was present in 90 of the 534 (16.9%). CONCLUSIONS: Diabetic retinopathy is correlated with the duration of diabetes, type of diabetes treatment, and fasting glucose level. Other factors have no significant association with the retinopathy. By multiple logistic analysis, duration of diabetes and fasting glucose level are the most important risk factors related to the retinopathy.

Adult↗