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Biomedical subjects

J Song

Publications and source records attributed to J Song.

At least 343 records · Page 19Linked to original sources
PubMed1994

The influence of surface properties on uptake of oil into complex coacervate microcapsules.

A range of surfactants with different hydrophile-lipophile balance (HLB) values was selected to investigate the influence of interfacial properties on the uptake of oil droplets into complex coacervate microcapsules. The well characterized gelatin/acacia complex coacervate system was used in this study and the encapsulation of squalane, and oleic acid was investigated. The surfactants investigated were Span 85, Span 80, Span 40, egg yolk lecithin, and Tween 80. Combinations of surfactants were utilized to obtain intermediate HLB values. The percentage oil encapsulated was determined gravimetrically, based on the initial concentration and the amount extracted from the microcapsules. The aqueous interfacial tension values of the oils and oil/surfactant systems were measured using the Wilhelmy plate method. The interfacial properties were correlated to the percentage oil uptake by the coacervate phase. The relative hydrophobicity/lipophilicity of the oil influenced its uptake by complex coacervate droplets. The presence of surfactant affected oil uptake, depending on the HLB value of the surfactant or surfactant mixture. Uptake of squalane by the gelatin/acacia coacervates was found to be optimized by the addition of surfactants with HLB values in the range 2.5-6. The percentage uptake of oil decreased rapidly for systems prepared containing surfactants with HLB values outside this range. No correlation was observed between oil uptake by the coacervate phase and the interfacial tension of the oil and oil/surfactant systems with double-distilled deionized water.

Capsules↗
PubMed1994

Evidence that v-Src-induced phospholipase D activity is mediated by a G protein.

v-Src-induced increases in diglyceride are derived from phosphatidylcholine via a type D phospholipase (PLD) and a phosphatidic acid phosphatase. v-Src-induced PLD activity, as measured by PLD-catalyzed transphosphatidylation of phosphatidylcholine to phosphatidylethanol, is inhibited by GDP beta S, which inhibits G-protein-mediated intracellular signals. Similarly, v-Src-induced increases in diglyceride are also blocked by GDP beta S. In contrast to the PLD activity induced by v-Src, PLD activity induced by the protein kinase C agonist, 12-O-tetradecanoylphorbol-13-acetate (TPA), was insensitive to GDP beta S. Consistent with the involvement of a G protein in the activation of PLD activity by v-Src, GTP gamma S, a nonhydrolyzable analog of GTP that potentiates G-protein-mediated signals, strongly enhanced PLD activity in v-Src-transformed cells relative to that in parental BALB/c 3T3 cells. The effect of GTP gamma S on PLD activity in v-Src-transformed cells was observed only when cells were prelabeled with [3H]myristate, which is incorporated exclusively into phosphatidylcholine, the substrate for the v-Src-induced PLD. There was no difference in the effect of GTP gamma S-induced PLD activity on v-Src-transformed and BALB/c 3T3 cells when the cells were prelabeled with [3H]arachidonate, which is not incorporated into phospholipids that are substrates for the v-Src-induced PLD. Similarly, GDP beta S inhibited PLD activity in v-Src-transformed cells much more strongly than in BALB/c 3T3 cells when [3H]myristate was used to prelabel the cells. The GTP-dependent activation of PLD by v-Src was dependent upon the presence of ATP but was unaffected by either cholera or pertussis toxin. These data suggest that v-Src induces PLD activity through a phosphorylation event and is mediated by a cholera and pertussis toxin-insensitive G protein.

3T3 Cells↗
PubMed1994

Influence of nuclear background on transcription of a chimeric gene (orf256) and coxI in fertile and cytoplasmic male sterile wheats.

Crosses between Triticum timopheevi, as maternal donor, and T. aestivum can lead to cytoplasmic male sterile (cms) plants. The T. timopheevi derived mitochondrial DNA from parental, cms, and fertility-restored lines differs from that of T. aestivum derived mtDNA in the coxI gene region. Our previous results for cms lines showed that there is an open reading frame, orf256, upstream from coxI in T. timopheevi derived mtDNA that is not present in T. aestivum DNA. The 5' flanking region and the first 33 nucleotides of the coding region of orf256 are identical to the corresponding region of T. aestivum coxI, whereas the rest of orf256, including the 3' flank, is not related to coxI. Also, the organization of orf256 and coxI on a HindIII fragment from T. timopheevi derived mtDNA are identical in T. timopheevi, cms, and fertility-restored lines. We now report that the DNA sequence of orf256 is identical in T. timopheevi, cms, and fertility-restored lines. Major transcripts in cms and fertility-restored lines encode both orf256 and coxI with 5' termini like coxI mRNA of T. aestivum, whereas parental mitochondria from T. timopheevi have major transcripts with 5' termini within the orf256 coding region. Mitochondria from cms and fertility-restored lines have the potential to produce a protein that would not be present in parental T. timopheevi or in T. aestivum.

Base Sequence↗
PubMed1994

Chloride and cation currents activated by bradykinin in coronary venular endothelial cells.

Bradykinin (BK) is known to activate several types of ion channels in endothelial cells, including a K+ channel and a nonselective cation channel. The predominant BK-activated current in most endothelial cells appears to be an outward, Ca(2+)-activated K+ current. We consistently recorded a rapidly activated, spontaneously inactivated inward current stimulated by BK in bovine coronary venular endothelial cells (CVECs). With the use of a whole cell, perforated patch recording mode, the average magnitude of the current was -293 +/- 38 pA. Simultaneous measurements of current and intracellular Ca2+ concentration ([Ca2+]i) showed that the inward current correlated closely with transient increases in [Ca2+]i due to Ca2+ release from intracellular stores. The current could be blocked by 4,4'-diisothiocyanatostilbene-2, 2'-disulfonic acid (DIDS) but not by La3+, and it persisted in Ca(2+)-free/Na(+)-free solution. When intra- and/or extracellular Cl- concentrations were altered, the reversal potential of the current shifted according to the calculated Cl- -equilibrium potential, indicating that the current was carried primarily by Cl-. Another inward current was also activated by BK. This current was slower to activate, could be blocked by La3+, but was not blocked by DIDS. The time course of the slowly activated current correlated with the plateau phase of the BK-stimulated [Ca2+]i increase, which was similar to the behavior of a nonselective cation current reported previously. We propose that these two currents may contribute to the depolarizations and net inward currents induced by BK in this cell line.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

Pituitary and hypothalamic somatostatin receptor subtype messenger ribonucleic acid expression in the food-deprived and diabetic rat.

Prolonged food deprivation (FD) and streptozocin-induced diabetes (STZ diabetes) in the rat result in abolition of GH secretory episodes. We have previously shown that hypothalamic prepro-GRF messenger RNA (mRNA) expression is markedly reduced in the hypothalamus of FD and STZ diabetic rats, with no change in prepro-somatostatin (SRIF) mRNA and suggested that reduced GRF and increased SRIF tone explained the loss of GH secretion in FD and STZ diabetes. Altered SRIF peptide expression has been implicated in many physiological and pathological states; however, information on the regulation of SRIF receptor (SSTR) expression is lacking. Therefore, we examined the expression of mRNA for the five recently cloned SSTR subtypes in the pituitary and hypothalamus of FD and STZ diabetic rats. In addition, we measured SRIF binding to pituitary membranes of FD rats. SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 80% in the pituitary of FD rats vs. fed controls, whereas pituitary levels of SSTR4 and SSTR5 mRNA were unaffected. The pituitary plasma membrane SSTR concentration was reduced over 50% in FD vs. fed animals. However, hypothalamic levels of the five isoforms were unchanged. In STZ diabetes, pituitary SSTR1, SSTR2, and SSTR3 mRNA expression was reduced 50-80%, with levels of SSTR1 partially restored by insulin, whereas SSTR4 mRNA was unchanged. In contrast to the effect of FD, SSTR5 mRNA levels were reduced 70% in the pituitary and 30% in the hypothalamus of STZ diabetic rats, with complete restoration by insulin. Thus, SSTR subtype mRNA expression is differentially regulated in two models of GH deficiency in the rat, FD and STZ diabetes. As chronic exposure to SRIF results in desensitization of transfected SSTR2 and SSTR3, and SSTR binding is decreased in FD and STZ diabetic rats, the possibility exists that the pituitary changes result from continued exposure to SRIF. In the hypothalamus, however, regulation appears more complex. These data support a role of increased SRIF with decreased GRF in mediating the loss of GH secretion in FD and diabetes.

Animals↗
PubMed1994

Distribution of carbohydrate epitopes among disjoint subsets of leech sensory afferent neurons.

Carbohydrate recognition plays an important role in the development of normal projections of sensory afferent neurons in the leech CNS. Four different carbohydrate epitopes are expressed by sensory afferents on their 130 kDa surface proteins: all sensory afferents share a common carbohydrate epitope (CE0) that helps them to enter and project diffusely across the synaptic neuropil; a restricted expression of three other carbohydrate epitopes (CE1, CE2, and CE3) serves to distinguish three subsets of sensory afferents. We examined the subsets of sensory afferents defined by their subset carbohydrate epitopes in the leech lip, skin, gut, and CNS. We established that the CE1, CE2, and CE3 subset epitopes define disjoint subsets of neurons by double labeling sensory afferents with monoclonal antibodies for different pairs of subset epitopes. We found that CE2 and CE3 afferents populate the lip and skin, but not the gut, and that these two subsets of sensory afferents have convergent projection patterns in the CNS. We found that CE1 afferents populate the gut and skin, but not lips; furthermore, their CNS projections diverge from those of CE2 and CE3 afferents. Our data fit the hypothesis that these carbohydrate epitopes are related to sensory modality of afferent subsets.

Animals↗
PubMed1994

The efficacy of Japanese encephalitis vaccine in Henan, China: a case-control study.

A population based case-control study to evaluate Japanese encephalitis (JE) vaccine efficacy was carried out in Gusi County, Henan Province, China from June to September in 1991. This study showed that the JE vaccine had a strong protective effect. The estimate of the vaccine efficacy was 78% (95% CI = 16-94%). An unimmunized child was at 4.54 times greater risk of developing JE than were fully immunized children during the study period. The present study may have underestimated the vaccine efficacy due to evaluation based on routine vaccination which might have been affected by vaccination management and the local cold chain system.

Antibodies, Viral↗
PubMed1994

[Repair of heel defect with a free medial plantar flap].

The results of reconstruction of plantar heel defects with a local random flap or an island medial plantar flap have in a majority of cases been satisfactory. However, in cases of extensive plantar defects, local tissue transfers are almost impossible. Since 1988, 8 cases with extensive plantar defects have been treated using free medial plantar cutaneous or musculocutaneous flaps. All flaps survived. Six weeks postoperatively, full weight-bearing was obtained and normal activities were resumed. No ulceration in the flaps has been noted in the follow up period between 6 and 24 months, and the two point discrimination was from 20 to 24 mm. The paper particularly points out the importance of nerve repair in the reconstruction, because recovery of the protective sensation is the most important factor to prevent plantar ulceration, and is the basis for good operative results.

Adolescent↗
PubMed1994

Epidermal growth factor induces the production of biologically distinguishable diglyceride species from phosphatidylinositol and phosphatidylcholine via the independent activation of type C and type D phospholipases.

An early response to epidermal growth factor in A431 cells is the generation of diglyceride, a physiological activator of protein kinase C. By differentially prelabeling cellular phospholipids with [3H]arachidonate and [3H]myristate, which are incorporated primarily into phosphatidylinositol and phosphatidylcholine, respectively, we have found that epidermal growth factor induces an increase in diglyceride levels from both phosphatidylinositol and phosphatidylcholine via distinct mechanisms and kinetics. The epidermal growth factor-induced increase in phosphatidylinositol-derived diglyceride was transient and peaked at 5 min. As diglyceride levels dropped, there was a corresponding increase in phosphatidic acid, suggesting that the diglyceride is efficiently converted to phosphatidic acid by a diglyceride kinase. In contrast, epidermal growth factor-induced increases in phosphatidylcholine-derived diglyceride peaked at 30 min and remained elevated for greater than 2 h. The epidermal growth factor-induced increases in phosphatidic acid detected in [3H]myristate-prelabeled cells paralleled the increase in diglyceride, suggesting that the phosphatidylcholine-derived diglyceride is produced from phosphatidic acid via a phosphatidic acid phosphatase. Consistent with this hypothesis, epidermal growth factor also induced a protein kinase C-independent phospholipase D activity that was specific for phosphatidylcholine. These data suggest that epidermal growth factor induces diglyceride production from phosphatidylinositol and phosphatidylcholine via two distinct mechanisms: a rapid and transient induction of diglyceride that likely involves phospholipase c-gamma-mediated hydrolysis of phosphatidylinositol-4,5-bisphosphate and a slower, more sustained induction of diglyceride via a phospholipase D-mediated hydrolysis of phosphatidylcholine to produce phosphatidic acid, which is then converted to diglyceride by a phosphatidic acid phosphatase.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaloids↗
PubMed1993

v-Src activates a unique phospholipase D activity that can be distinguished from the phospholipase D activity activated by phorbol esters.

Phospholipase D (PLD) activity, as measured by the transphosphatidylation of cellular phospholipids, is elevated in BALB/c 3T3 cells transformed by v-Src. Phorbol esters that activate protein kinase C (PKC) also increase PLC activity in BALB/c 3T3 cells. v-Src-induced PLD activity could be distinguished from phorbol ester-induced PLD activity by differential radiolabelling of phospholipids, which are the substrates of PLD. Both v-Src- and phorbol ester-induced PLD activity could be detected when phospholipids were prelabelled with either radiolabelled myristate or palmitate; however, only phorbol ester-induced PLD activity could be detected when either arachidonate or 1-O-alkyl-sn-glyceryl-3-phosphorylcholine (alkyl-lysoPC) was used to prelabel the phospholipids. The increased PLD activity in v-Src-transformed cells was not detected when the cells were prelabelled with either arachidonic acid or alkyl-lysoPC, which contains an ether linkage at sn-1 of the glycerol backbone. As both arachidonic acid and alkyl-lysoPC are incorporated into phosphatidylcholine (PC), the substrate for v-Src-induced PLD activity, these data suggest that the PLD activated by v-Src can distinguish PCs lacking arachidonic acid and ether linkages. Consistent with v-Src activating a PLD activity that is distinct from that activated by phorbol esters that activate PKC directly, neither depleting cells of PKC nor treatment with the protein kinase inhibitor, staurosporine, had any effect on v-Src-induced PLD activity, whereas both PKC depletion and staurosporine inhibited phorbol ester-induced PLD activity. Taken together, these data suggest that v-Src activates a PKC-independent PLD activity that is specific for a subpopulation of PC and distinct from the PLD activity induced by PKC activity induced by phorbol esters. The diacylglycerol produced from PC by the action of the v-Src-induced PLD may therefore be responsible for the activation of PKC by v-Src.

3T3 Cells↗
PubMed1993

Molecular cloning and sequencing of a human somatostatin receptor, hSSTR4.

We recently reported the cloning of a somatostatin receptor (SSTR) subtype from a rat genomic library designated rSSTR4. In the present study, we report the cloning of the human SSTR4 gene. A human genomic library was screened with a 1.2 kb fragment of rSSTR4 containing the full open reading frame and a genomic clone, hSSTR4, was isolated. The deduced amino acid sequence of this clone encoded a protein of 388 amino acids and is a member of the G-protein coupled receptor superfamily. Comparison of rat and human SSTR4 sequences demonstrated 89% identity. In addition, the sequence of hSSTR4 shows 61%, 46%, and 47% sequence identity with previously identified isoforms hSSTR1, hSSTR2, and hSSTR3, respectively.

Amino Acid Sequence↗
PubMed1993

A dominant negative Raf-1 mutant prevents v-Src-induced transformation.

A vector expressing a dominant negative mutant of Raf-1 was stably introduced into BALB/c 3T3 cells expressing a temperature-sensitive derivative of v-Src. High levels of the Raf-mutant were detected in these cells. Expression of the Raf-1 mutant blocked v-Src-induced transformation, as determined by reversion to a flat non-transformed morphology and the inability to form colonies in soft agar. Cells transfected with the parental vector lacking the mutant Raf-1 could be transformed by v-Src. These data suggest that intracellular signals activated by v-Src that are mediated by Raf-1 are required for transformation by v-Src.

3T3 Cells↗
PubMed1993

Cytoplasmic male sterility and fertility restoration in wheat are not associated with rearrangements of mitochondrial DNA in the gene regions for cob, coxII, or coxI.

In comparing the genetic organization and exploring the molecular basis of cytoplasmic male sterility (CMS) in wheat, mitochondrial DNAs (mtDNA) from Triticum aestivum, T. timopheevi, CMS alloplasmic wheat with T. aestivum nucleus and T. timopheevi mitochondria, and fertility-restored lines were compared by hybridization analysis with specific probes for three gene regions: coxII, cob, and coxI. Minor differences between T. aestivum- and T. timopheevi-derived sources were found for gene regions for coxII and cob. For coxI, there are significant differences between T. timopheevi-derived mtDNAs and T. aestivum mtDNA extending beyond an 8 kb distance. All T. timopheevi-derived mtDNA sources have a chimeric gene region (orf256) with part of the upstream coxI gene region, including some coxI-coding region, preceding coxI. The part of orf256 that does not include any of coxI and the 3'-flanking region of CMS coxI are not found in T. aestivum mtDNA. Neither orf256 nor the CMS 3'-flanking region of coxI are found in T. timopheevi or T. aestivum chloroplastic or nuclear DNA. There do not appear to be DNA sequence differences for the three gene regions studied that are related to either CMS or fertility-restored states.

Blotting, Southern↗
PubMed1993

Pituitary and hypothalamic insulin-like growth factor-I (IGF-I) and IGF-I receptor expression in food-deprived rats.

The present study was designed to evaluate a possible role for the insulin-like growth factor-I (IGF-I) system in mediating the suppression of growth hormone (GH) secretion observed in food-deprived rats by measuring IGF-I mRNA, receptor concentration and receptor mRNA in neuroendocrine tissues (hypothalamus and pituitary). Rats were deprived of food (food-deprived) for 72 h or had free access to food (fed). Tissues were processed for measurement of steady-state levels of: (a) IGF-I and IGF-I receptor mRNA (by solution hybridization/RNase protection assay); (b) IGF-I in serum and tissue extracts (by RIA) and (c) IGF-I displaceable [125I]IGF-I binding to plasma membrane preparations. Food deprivation resulted in decreased serum and liver levels of IGF-I. Kidney IGF-I mRNA levels were reduced 80% in food-deprived rats with a concomitant increase in IGF-I receptor concentration and mRNA levels. Refeeding of food-deprived rats fully normalized these perturbations. Pituitary IGF-I content was reduced 50% in food-deprived rats while IGF-I mRNA levels were unaffected. A modest increase was seen in pituitary IGF-I receptor concentration; however, IGF-I receptor mRNA levels were not changed. Hypothalamic IGF-I mRNA content was reduced in 72 h food-deprived rats while IGF-I receptor binding capacity and mRNA were unaffected. In conclusion, IGF-I mRNA levels are decreased in liver, kidney and hypothalamus together with a reduction in plasma IGF-I in food-deprived rats but is unaffected in anterior pituitary. IGF-I receptor gene expression and binding capacity are coordinately regulated in kidney and hypothalamus, but not in the pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Bending rigidity of SOPC membranes containing cholesterol.

Bilayer membranes in the fluid state exhibit a large resistance to changes in surface area, negligible resistance to surface shear deformation, and a small but finite resistance to bending. The presence of cholesterol in the membrane is known to increase its resistance to area dilation. In this report, a new method for measuring bilayer membrane bending stiffness has been used to investigate the effect of cholesterol on the bending rigidity of SOPC (1,stearoyl-2,oleoyl-phosphatidylcholine) membranes. The curvature elasticity (kc) for membranes saturated with cholesterol was measured to be 3.3 x 10(-19) J, approximately 3-fold larger than that the modulus for cholesterol-free SOPC membrane. These findings are consistent with previous measurements of bending stiffness based on thermal fluctuations, which showed a similar approximately 3-fold increase in the modulus with cholesterol addition (Evans and Rawicz, 1990, Phys. Rev. Lett. 64:2094) and provide further substantiation of the important contribution that cholesterol makes to membrane cohesion and stability.

Cholesterol↗
PubMed1993

The aroQ-encoded monofunctional chorismate mutase (CM-F) protein is a periplasmic enzyme in Erwinia herbicola.

Enteric bacteria possess two species of chorismate mutase which exist as catalytic domains on the amino termini of the bifunctional PheA and TyrA proteins. In addition, some of these organisms possess a third chorismate mutase, CM-F, which exists as a small monofunctional protein. The CM-F gene (denoted aroQ) from Erwinia herbicola was cloned and sequenced for the first time. A strategy for selection by functional complementation in a chorismate mutase-free Escherichia coli background was devised by using a recombinant plasmid derivative of pUC18 carrying a Zymomonas mobilis tyrC insert which encodes cyclohexadienyl dehydrogenase. The aroQ gene is 543 bp in length, predicting a 181-residue protein product having a calculated molecular mass of 20,299 Da. The E. herbicola aroQ promoter is recognized by E. coli, and a putative sigma-70 promoter region was identified. N-terminal amino acid sequencing of the purified CM-F protein indicated cleavage of a 20-residue signal peptide. This was consistent with the monomeric molecular mass determined for the enzyme of about 18,000 Da. The native enzyme is a homodimer. The implied translocation of CM-F was confirmed by osmotic shock experiments which demonstrated a periplasmic location. Immunogold electron microscopy indicated a polar localization within the periplasm. Polyclonal antibody raised against E. herbicola CM-F did not cross-react with the CM-F protein from the closely related Serratia rubidaea, as well as from a number of other gram-negative bacteria. Furthermore, when the E. herbicola aroQ gene was used as a probe in Southern blot hybridizations with EcroRI digests of chromosomal DNA from S. rubidaea and other enteric organisms, no hybridization was detected at low stringency. Thus, the aroQ gene appears to be unusually divergent among closely related organisms. The deduced CM-F amino acid sequence did not exhibit compelling evidence for homology with the monofunctional chorismate mutase protein of Bacillus subtilis.

Amino Acid Sequence↗
PubMed1993

Vif is crucial for human immunodeficiency virus type 1 proviral DNA synthesis in infected cells.

The human immunodeficiency virus type 1 (HIV-1) vif gene encodes a 23-kDa protein of unknown function, also produced by most other known lentiviruses. Vif was found to be essential for the spread of HIV-1 in peripheral blood lymphocytes and in primary macrophages, as well as in some but not all established T-cell lines. Vif was required at the stage of viral particle formation, for cell-to-cell as well as for cell-free transmission of HIV-1. Accordingly, vif-defective viruses could be complemented by the expression of vif in the producer but not in the target cell. vif-defective virions contained wild-type amounts of Gag and Env proteins, reverse transcriptase, integrase, genomic RNA, and partial reverse transcripts. Most importantly, they could enter cells normally, and the vif defect could not be rescued through the use of HIV(MLV [murine leukemia virus]) pseudotypes. Instead, vif-mutant viruses were severely impaired in their ability to complete the synthesis of proviral DNA, once internalized in the target cell. These results suggest that Vif plays a role which is novel for a retroviral protein, in allowing the processing and/or the transport of the internalized HIV core.

Amino Acid Sequence↗