Search PubMed⌕ Search

Biomedical subjects

Y Song

Publications and source records attributed to Y Song.

At least 145 records · Page 8Linked to original sources

Ion-pair formation observed in a pulsed-field ionization photoelectron spectroscopic study of HF

The pulsed-field ionization (PFI) photoelectron (PE) spectrum of HF has been recorded at the chemical dynamics beamline of the advanced light source over the photon energy range 15.9-16.5 eV using a time-of-flight selection scheme at a resolution of 0.6 meV. Rotationally-resolved structure in the HF+(X 2 pi 3/2, 1/2, v+ = 0, 1) band systems are assigned. The spectral appearance of these systems agrees with a previous VUV laser PFI-PE study. Importantly, extensive rotationally-resolved structure between these two vibrational band systems is also observed. This is attributed to ion-pair formation via Rydberg states converging on the v+ = 1 vibrational levels of the HF+(X 2 pi 3/2, 1/2) spin-orbit states. These Rydberg states are assigned to the 1 sigma+ part of the nd-complexes (sigma, pi, and delta). Ion-pair formation is observed in this study by the detection of F- ions. Some partially rotationally-resolved structure in a previously published threshold photoelectron spectrum is similarly attributed to ion-pair formation (F- detection) through a combination of the v+ = 17 level of the (A 2 sigma+) 3s sigma Rydberg state and the (X 2 pi 3/2, 1/2, v+ = 1) 7d Rydberg states. On the basis of the present study, an accurate experimental value for the dissociation energy of the ground state of HF has been obtained, D0(HF) = 5.8650(5) eV.

Journal Article↗

Pulsed field ionization-photoelectron photoion coincidence spectroscopy with synchrotron radiation: the heat of formation of the C2H5+ ion

Pulsed field ionization photoelectron (PFI-PE) spectroscopy combined with ion coincidence detection has been used with multi-bunch synchrotron radiation at the Advance Light Source (ALS) to energy select ions and to measure their breakdown diagram. The resolution for ion state selection achieved with Ar+ (2P3/2, 1/2) employing this PFI-PE-photoion coincidence apparatus is 0.6 meV (full width at half maximum). The production of C2H5+ from C2H5Br was investigated near the dissociative photoionization limit with this pulsed field ionization-threshold photoelectron photoion coincidence (PFI-PEPICO) scheme. Although the PFI-PE spectra of C2H5Br, C2H5I, and benzene show that the production of ions in the Franck-Condon gap regions is quite low, the selectivity for PFI-PE detection and the suppression of prompt electrons is such that we can detect 1 PFI-PE out of 25,000 total electrons s-1. The derived C2H5+ heat of formation from the analysis of the C2H5Br+ breakdown diagram and a critical analysis of other results is 900.5 +/- 2.0 kJ mol-1 at 298 K, or 913.2 +/- 2.0 kJ mol-1 at 0 K. This leads to an ethylene proton affinity at 298 K of 682.0 kJ mol-1. The measured IE of C2H5Br is 10.307 eV.

Journal Article↗

Dysregulated production of interferon-gamma, interleukin-4 and interleukin-6 in early tuberculosis patients in response to antigen 85B of Mycobacterium tuberculosis.

Both interferon-gamma (IFN-gamma) and interleukin (IL)-4 expression in T cells and IL-6 expression in cells of the monocyte/macrophage lineage were monitored using antigen 85B (Ag85B) protein and purified protein derivative (PPD) antigen in the early stages of tuberculosis (TB). We showed that the levels of cell-associated IFN-gamma and IL-4 (mRNA and intracellular cytokine) in Ag85B-stimulated T cells were significantly depressed in TB patients compared with those in healthy tuberculin reactors. On the other hand, the capacity of peripheral blood mononuclear cells (PBMC) to produce IL-6 spontaneously ex vivo was enhanced in patients (P < 0. 001), but their corresponding capacities to respond to Ag85B were not significantly different from those of normal donors. After 2 months of antituberculosis therapy, the mean blastogenic responses of Ag85B-stimulated PBMC from seven TB patients were increased 6. 1-fold (P = 0.011). Furthermore, the proportions of both IFN-gamma- (P < 0.01) and IL-4- (P = 0.05) producing T cells were significantly increased. However, those of IL-6-producing cells were diminished in response to Ag85B (P = 0.05). Our results suggest that there may be an altered regulation of IFN-gamma, IL-4 and IL-6 to Ag85B in the early stages of TB.

Acyltransferases↗

Role of aquaporin-4 in airspace-to-capillary water permeability in intact mouse lung measured by a novel gravimetric method.

The mammalian peripheral lung contains at least three aquaporin (AQP) water channels: AQP1 in microvascular endothelia, AQP4 in airway epithelia, and AQP5 in alveolar epithelia. In this study, we determined the role of AQP4 in airspace-to-capillary water transport by comparing water permeability in wild-type mice and transgenic null mice lacking AQP1, AQP4, or AQP1/AQP4 together. An apparatus was constructed to measure lung weight continuously during pulmonary artery perfusion of isolated mouse lungs. Osmotically induced water flux (J(v)) between the airspace and capillary compartments was measured from the kinetics of lung weight change in saline-filled lungs in response to changes in perfusate osmolality. J(v) in wild-type mice varied linearly with osmotic gradient size (4.4 x 10(-5) cm(3) s(-1) mOsm(-1)) and was symmetric, independent of perfusate osmolyte size, weakly temperature dependent, and decreased 11-fold by AQP1 deletion. Transcapillary osmotic water permeability was greatly reduced by AQP1 deletion, as measured by the same method except that the airspace saline was replaced by an inert perfluorocarbon. Hydrostatically induced lung edema was characterized by lung weight changes in response to changes in pulmonary arterial inflow or pulmonary venous outflow pressure. At 5 cm H(2)O outflow pressure, the filtration coefficient was 4.7 cm(3) s(-1) mOsm(-1) and reduced 1.4-fold by AQP1 deletion. To study the role of AQP4 in lung water transport, AQP1/AQP4 double knockout mice were generated by crossbreeding of AQP1 and AQP4 null mice. J(v) were (cm(3) s(-1) mOsm(-1) x 10(-5), SEM, n = 7-12 mice): 3.8 +/- 0. 4 (wild type), 0.35 +/- 0.02 (AQP1 null), 3.7 +/- 0.4 (AQP4 null), and 0.25 +/- 0.01 (AQP1/AQP4 null). The significant reduction in P(f) in AQP1 vs. AQP1/AQP4 null mice was confirmed by an independent pleural surface fluorescence method showing a 1.6 +/- 0.2-fold (SEM, five mice) reduced P(f) in the AQP1/AQP4 double knockout mice vs. AQP1 null mice. These results establish a simple gravimetric method to quantify osmosis and filtration in intact mouse lung and provide direct evidence for a contribution of the distal airways to airspace-to-capillary water transport.

Animals↗

Sutural expansion osteogenesis for management of the bony-tissue defect in cleft palate repair: experimental studies in dogs.

A series of experimental studies on sutural expansion osteogenesis for management of the bony-tissue defect in cleft palate repair was performed between 1995 and 1997. Forty-five young dogs in weaning were used in four experiments that were divided into two parts. Part I probed the possibility of closing the surgically constructed hard palate cleft not only with mucoperiosteum but also with bony tissue by the technique of sutural expansion of lateral palatine sutures. Part II explored the possibility of pushing the palatine bone posteriorly and advancing the maxillary segment anteriorly by transverse palatine suture expansion. In Part I, a ring-shaped suture expander made of nickel-titanium shape memory alloy was used to expand the lateral suture of palatine bones. Expansion forces of 200 G, 360 G, and 480 G were used for the first experiment. A force of 360 G was chosen for two other experiments; this force is equivalent to the distraction rate of 0.5 mm per day of a jackscrew device. The ring-shaped suture expander was opened and its two feet were fixed in the medial sides of residual horizontal plates of the palatine bones immediately after a hard palate cleft was constructed surgically under endotracheal general anesthesia. At the eighth postoperative day, under the traction of 360 G, the two sides of the 8-mm-wide hard palate cleft were brought into contact with each other, and 8 or 9 days later the closed palatal cleft had healed completely with mucosal tissue. This experiment was repeated twice and yielded the same results. Sutural expansion osteogenesis was evaluated physically, fluorescently, histologically, and ultrastructurally to examine the deposition of the regenerated bone in the suture areas. Additionally, the influence of sutural expansion osteogenesis of the palatal bones on other facial bones was also studied cephalometrically. In Part II, a bow-shaped suture expander made of nickel-titanium shape memory alloy was applied to expand either the left or the right side of the transverse palatal suture of each of the experimental dogs. At the postoperative week 4 to 6, the maxillary segment was moved forward 5 to 6 mm on the expanded side, and the palatal bone was pushed backward 5 mm. The changes of bone position were assessed radiographically and cephalometrically. Tissue response of circum-maxillary sutures was examined histologically. These experiments led to the following conclusions: (1) Bony closure of the surgically constructed hard palate cleft with a ring-shaped suture expander made of nickel-titanium shape memory alloy is possible. (2) Anterior advancement of the maxillary segment and posterior lengthening of the hard palate using a bow-shaped suture expander made of nickel-titanium shape memory alloy applied at the palatomaxillary suture (transverse palatal suture) of the hard palate are also possible. Thus, in humans, a new approach for cleft palate repair may be a worthwhile investigation.

Alloys↗

Acetatodiaqua

Explore the source record for details and available documents.

Journal Article↗

Role of water channels in fluid transport studied by phenotype analysis of aquaporin knockout mice.

Aquaporin-type water channels are expressed widely in mammalian tissues, particularly in the kidney, lung, eye and gastrointestinal tract. To define the role of aquaporins in organ physiology, we have generated and analysed transgenic mice lacking aquaporins (AQP) 1, 3, 4 and 5. Multiple phenotype abnormalities were found in the null mice. For example, in kidney, deletion of AQP1 or AQP3 produced marked polyuria whereas AQP4 deletion produced only a mild concentrating defect. Deletion of AQP5, the apical membrane water channel in the salivary gland, caused defective saliva production. Deletion of AQP1 or AQP5, water channels in lung endothelia and epithelia, resulted in a 90% decrease in airspace-capillary water permeability. In the brain, deletion of AQP4 conferred marked protection from brain swelling induced by acute water intoxication and ischaemic stroke. The general paradigm that has emerged from these phenotype studies is that aquaporins facilitate rapid near-isosmolar transepithelial fluid absorption/secretion, as well as rapid vectorial water movement driven by osmotic gradients. However, we have found many examples in which the tissue-specific expression of an aquaporin is not associated with any apparent phenotypic abnormality. The physiological data on aquaporin null mice suggest the utility of aquaporin blockers and aquaporin gene replacement in selected human diseases.

Animals↗

Skeletal muscle function and water permeability in aquaporin-4 deficient mice.

It has been proposed that aquaporin-4 (AQP4), a water channel expressed at the plasmalemma of skeletal muscle cells, is important in normal muscle physiology and in the pathophysiology of Duchenne's muscular dystrophy. To test this hypothesis, muscle water permeability and function were compared in wild-type and AQP4 knockout mice. Immunofluorescence and freeze-fracture electron microscopy showed AQP4 protein expression in plasmalemma of fast-twitch skeletal muscle fibers of wild-type mice. Osmotic water permeability was measured in microdissected muscle fibers from the extensor digitorum longus (EDL) and fractionated membrane vesicles from EDL homogenates. With the use of spatial-filtering microscopy to measure osmotically induced volume changes in EDL fibers, half times (t(1/2)) for osmotic equilibration (7.5-8.5 s) were not affected by AQP4 deletion. Stopped-flow light-scattering measurements of osmotically induced volume changes in plasmalemma vesicles also showed no significant differences in water permeability. Similar water permeability, yet approximately 90% decreased AQP4 protein expression was found in EDL from mdx mice that lack dystrophin. Skeletal muscle function was measured by force generation in isolated EDL, treadmill performance time, and in vivo muscle swelling in response to water intoxication. No differences were found in EDL force generation after electrical stimulation [42 +/- 2 (wild-type) vs. 41 +/- 2 (knockout) g/s], treadmill performance time (22 vs. 26 min; 29 m/min, 13 degrees incline), or muscle swelling (2.8 vs. 2.9% increased water content at 90 min after intraperitoneal water infusion). Together these results provide evidence against a significant role of AQP4 in skeletal muscle physiology in mice.

Animals↗

Role of aquaporin water channels in pleural fluid dynamics.

Continuous movement of fluid into and out of the pleural compartment occurs in normal chest physiology and in pathophysiological conditions associated with pleural effusions. RT-PCR screening and immunostaining revealed expression of water channel aquaporin-1 (AQP1) in microvascular endothelia near the visceral and parietal pleura and in mesothelial cells in visceral pleura. Comparative physiological measurements were done on wild-type vs. AQP1 null mice. Osmotically driven water transport was measured in anesthetized, mechanically ventilated mice from the kinetics of pleural fluid osmolality after instillation of 0.25 ml of hypertonic or hypotonic fluid into the pleural space. Osmotic equilibration of pleural fluid was rapid in wild-type mice (50% equilibration in <2 min) and remarkably slowed by greater than fourfold in AQP1 null mice. Small amounts of AQP3 transcript were also detected in pleura by RT-PCR, but osmotic water transport was not decreased in AQP3 null mice. In spontaneously breathing mice, the clearance of isosmolar saline instilled in the pleural space ( approximately 4 ml. kg(-1). h(-1)) was not affected by AQP1 deletion. In a fluid overload model produced by intraperitoneal saline administration and renal artery ligation, the accumulation of pleural fluid (approximately 0.035 ml/h) and was not affected by AQP1 deletion. Finally, in a thiourea toxicity model of acute endothelial injury causing pleural effusions and lung interstitial edema, pleural fluid accumulation in the first 3 h ( approximately 4 ml. kg(-1). h(-1)) was not affected by AQP1 deletion. These results indicate rapid osmotic equilibration across the pleural surface that is facilitated by AQP1 water channels. However, AQP1 does not appear to play a role in clinically relevant mechanisms of pleural fluid accumulation or clearance.

Animals↗

Aquaporin water channels and lung physiology.

Fluid transport across epithelial and endothelial barriers occurs in the neonatal and adult lungs. Biophysical measurements in the intact lung and cell isolates have indicated that osmotic water permeability is exceptionally high across alveolar epithelia and endothelia and moderately high across airway epithelia. This review is focused on the role of membrane water-transporting proteins, the aquaporins (AQPs), in high lung water permeability and lung physiology. The lung expresses several AQPs: AQP1 in microvascular endothelia, AQP3 in large airways, AQP4 in large- and small-airway epithelia, and AQP5 in type I alveolar epithelial cells. Lung phenotype analysis of transgenic mice lacking each of these AQPs has been informative. Osmotically driven water permeability between the air space and capillary compartments is reduced approximately 10-fold by deletion of AQP1 or AQP5 and reduced even more by deletion of AQP1 and AQP4 or AQP1 and AQP5 together. AQP1 deletion greatly reduces osmotically driven water transport across alveolar capillaries but has only a minor effect on hydrostatic lung filtration, which primarily involves paracellular water movement. However, despite the major role of AQPs in lung osmotic water permeabilities, AQP deletion has little or no effect on physiologically important lung functions, such as alveolar fluid clearance in adult and neonatal lung, and edema accumulation after lung injury. Although AQPs play a major role in renal and central nervous system physiology, the data to date on AQP knockout mice do not support an important role of high lung water permeabilities or AQPs in lung physiology. However, there remain unresolved questions about possible non-water-transporting roles of AQPs and about the role of AQPs in airway physiology, pleural fluid dynamics, and edema after lung infection.

Animals↗

Lung fluid transport in aquaporin-5 knockout mice.

The mammalian lung expresses water channel aquaporin-1 (AQP1) in microvascular endothelia, AQP4 in airway epithelia, and AQP5 at the apical plasma membrane in type I cells of alveolar epithelia. We previously studied the role of AQP1 and AQP4 in lung fluid transport using knockout mice. Here, we examined the role of AQP5 using AQP5 knockout mice, which were recently shown to manifest defective saliva secretion. AQP5 deletion did not affect lung morphology at the light microscopic level, nor did it affect the distribution or expression of aquaporins 1, 3, or 4. Airspace-capillary osmotic water permeability (P(f)) was measured in isolated perfused lungs by pleural surface fluorescence and gravimetric methods. P(f) was reduced 10-fold by AQP5 deletion and was further reduced by 2- to 3-fold in AQP1/AQP5 double-knockout mice. Hydrostatic lung edema in response to acute increases in pulmonary artery pressure was not affected by AQP5 deletion. Active alveolar fluid absorption was measured in an in situ lung model from the increase in concentration of a volume marker in an isosmolar alveolar instillate. Interestingly, fluid absorption did not differ in litter-matched AQP5 knockout mice, nor was there an effect of AQP5 deletion when fluid absorption was maximally stimulated by pretreatment of mice with keratinocyte growth factor. These results indicate that AQP5 is responsible for the majority of water transport across the apical membrane of type I alveolar epithelial cells. The unimpaired alveolar fluid clearance in AQP5-null mice indicates that high alveolar water permeability is not required for active, near-isosmolar fluid transport.

Animals↗

A method of "unilateral operation" for early repair of unilateral complete cleft palate. Preliminary report.

OBJECTIVE: This article describes a method of "unilateral operation" and the preliminary results of a group of patients with unilateral complete cleft palate undergoing the operation at early age. DESIGN: The "unilateral operation" consists of four relaxation maneuvers. After all of the four maneuvers have been performed on the deformed side of an unilateral complete cleft palate, the deformed side can be moved posteriorly and medially to contact with the normal side. Then the cleft can be closed without tension. RESULTS: From 1995 to 1998, 19 cases of unilateral complete cleft palate were repaired with this method at 5-12 months of age. Postoperatively, there were no deaths nor dehiscences. Under the care and guidance of an experienced speech pathologist, 15 of 17 of these children have normal vocal quality at 1-2 years of age. CONCLUSIONS: The "unilateral operation" is a rational, adequate, and safe method for early repair of unilateral complete cleft palate. It's design addresses four principles. First, operating only on the deformed side of a unilateral complete cleft palate leaves the normal side unperturbed. Second, complete relaxation of the deformed side is achieved before closing the cleft. Third, in comparison with conventional procedures, which operate on both sides of the palate, this method has the advantage of less surgical trauma, less blood loss, and shorter time of operation. Fourth, all of these advantages are beneficial to early cleft palate repair, which is an important factor in achieving good speech.

Anesthesia, General↗

Inhibition of RNA polymerase I transcription in differentiated myeloid leukemia cells by inactivation of selectivity factor 1.

Transcription by RNA polymerase I (pol I) regulates the rate of ribosome biogenesis and the biosynthetic potential of the cell; therefore, it plays an important role in the control of cell growth. Differentiation of the human promyelocytic leukemic cell line U937 is accompanied by drastic decreases in pol I transcriptional activity. We have used cell-free extracts prepared from undifferentiated and differentiated U937 cells to investigate the molecular mechanisms responsible for this inhibitory process. Our analysis indicates that the activity of the TATA binding protein (TBP)/TBP-associated factor (TAF) complex selectivity factor 1 (SL1), one of the factors required for accurate and promoter-specific transcription by RNA pol I, is severely repressed in differentiated U937 cells. Moreover, the reduction in SL1 activity is not a consequence of a decrease in SL1, because there is no detectable difference in the abundance of TBP or TAFs before and after U937 cell differentiation. In conclusion, our results indicate that the selectivity factor SL1 is an important target for the regulation of pol I transcription during cell differentiation.

Cell Differentiation↗

A wild-type sequence p53 peptide presented by HLA-A24 induces cytotoxic T lymphocytes that recognize squamous cell carcinomas of the head and neck.

Evidence has accumulated indicating that HLA-A2-restricted CTLs specific for human wild-type sequence p53 epitopes lyse tumor cells expressing mutant p53. To explore the possibility that wild-type sequence p53 peptides could also be used in vaccines for patients expressing HLA-A24 antigen, another frequent HLA class I allele, we investigated the induction of HLA-A24-restricted p53-specific CTLs from the peripheral blood lymphocytes of normal donors. Of six p53-derived peptides possessing an HLA-A24 binding motif, the p53 peptide 125-134 (p53(125-134)) was found to have a high binding capacity and induced peptide-specific CTLs from peripheral blood mononuclear cells, using peptide-pulsed autologous dendritic cells and subsequent cultivation with cytokines interleukin 2 and interleukin 7. Bulk CTL populations lysed peptide-pulsed HLA-A24+ targets as well as HLA-A24+ squamous cell carcinoma of the head and neck (SCCHN) cell lines. However, IFN-gamma pretreatment of HLA-A24+ SCCHN cell lines was necessary for lysis, suggesting that a ligand density higher than that normally expressed by tumor cells is required for these CTLs to mediate lysis. Moreover, a cloned CTL, designated TH#99, isolated from the bulk population by limiting dilution, lysed HLA-A24+ SCCHN targets more efficiently than the bulk CTL population. Lysis was inhibited by anti-HLA class I monoclonal antibody but not by anti-HLA-DR monoclonal antibody. These results indicate that HLA-A24-restricted CTLs recognizing the wild-type sequence p53(125-134) can be generated using autologous dendritic cells from precursors present in peripheral blood lymphocytes obtained from normal HLA-A24+ donors. This finding suggests that vaccine strategies targeting wild-type sequence p53 epitopes can be extended to a wider range of cancer patients.

Amino Acid Sequence↗

[Selection of high avermectins producing strain and identification of avermectin B1].

Three types of colony, powdery gray, white and bald, were isolated from Streptomyces avermitilis ATCC31272. Among them, only the powdery grey one produces avermectins. Sa-76 strain was selected from the powdery grey strain by mutation with high energy electric flow, and its avermectins titer attainde 100 micrograms/mL in shaking flask. Avermectin B1 was extracted and purified from the mycelia of Sa-76, and identified by UV, IR, 1H-NMR, 13C-NMR and mass spectra. After Sa-76 strain was treated twice with NTG, a strain named Sa-76-8 was selected with avermectins titer over 2000 micrograms/mL. The Sa-76-8 strain was treated with NTG once again, and a high avermectins producing strain named as Sa-76-9 with avermectins titer up to 3500-4000 micrograms/mL was selected.

Anthelmintics↗

[The effect of polylactide screws on fracture healing].

This experiment aimed at investigating the effect of a kind of home-bred poly-DL-lactide screws on fracture healing. An operation was performed so as to make bilateral lateral condylar fractures of the femur in 8 dogs. The left sides were fixed with 2 home-bred PDLLA(Mv = 43 x 10(4)) screws, and the contralateral sides were fixed with 2 metalic screws to be used as controls. The animals were sacrificed at 2, 4, 8, and 12 weeks after surgery. Optic microscopy and SEM photography were done. The results of optic microscopy showed that fibrous callus formed already in both groups by 2 weeks after surgery, and bilateral fractures united uneventfully by 12 weeks. Although the course of fracture healing in experimental group was slower than that in control group, the osteogenesis in experimental group appeared to be normal. The SEM examination demonstrated that collagenous fibers arranged regularly and calcified normally in both groups at 12 weeks. And many square and rhomboid granules produced from the degradation of PDLLA material were found in experimental group at 12 weeks. Therefore, it is suggested that this kind of home-bred PDLLA screws should be applicable to fractures where the tissues are rich in blood supply.

Animals↗