Search PubMed⌕ Search

Biomedical subjects

Y Huang

Publications and source records attributed to Y Huang.

At least 1,027 records · Page 57Linked to original sources
PubMed1994

Cloning the ribosomal RNA operons of Mycoplasma flocculare and comparison with those of Mycoplasma hyopneumoniae.

In contrast to other mycoplasma species the 16S/23S rRNA and 5S rRNA operons of Mycoplasma flocculare and Mycoplasma hyopneumoniae map at least 150 kb apart (20% of the genome). Both operons from M. flocculare have been cloned and sequenced. The 23S rRNA gene sequence showed 96.7% homology with the corresponding gene of M. Hyopneumoniae, equalling that found earlier for 16S rRNA and confirming the close phylogenetic relationships of these organisms. A possible upstream promoter was identified. Sequence elements upstream and downstream from each structural gene could form a stem needed for maturation of the immature rRNA transcript to mature 16S and 23S rRNA. We also identified two possible stem-and-loop sequences 3' to the 23S rRNA gene. The 5S rRNA gene itself also showed high homology with the corresponding structural gene of M. hyopneumoniae, although the upstream and downstream sequences were highly heterologous.

Base Sequence↗
PubMed1994

A MADYMO model of near-side human occupants in side impacts.

The protection of automotive occupants against broadside collisions is of current interest due to the implementation of a new Federal standard on side impact. There is controversy as to the validity of the standard, the best criterion to assess injury to the thorax and the type and manner in which padding should be used. Although it has been shown in a series of 17 cadaveric tests that paper honeycomb can reduce thoracic injuries dramatically, there are still concerns regarding the loss of air space between the door and the occupant due to the presence of the padding and regarding the loss of protection for the thorax when there is no engagement of the shoulder with the intruding side structure of the car. This paper describes the development of a three-dimensional rigid body model to simulate cadaveric experiments carried out at Wayne State University. Model parameters were chosen to yield human-like responses at the level of the shoulder, thorax, abdomen and pelvis. The model was then used to study the effect of padding on injury parameters related to the nearside occupant when a relatively thick padding is used (up to 100 mm). It was also used to study the increase in force on the thorax when shoulder engagement is lost. Laboratory tests were conducted with full shoulder engagement but in the field most cars have a low beltline (window sill) which effectively eliminates shoulder contact if the arms are outstretched in a normal driving posture. If a sufficiently soft padding was used, the model did not predict an increase in thoracic force level or any of the injury parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗
PubMed1994

A fiber matrix model for the growth of macromolecular leakage spots in the arterial intima.

A new model is presented for the growth of cellular level macromolecular leakage spots in the arterial intima. The theoretical approach differs from the recent study by Yuan et al. [19] in that it directly models and calculates the intimal transport parameters based on Frank and Fogelman's [22] ultrastructural observations of the extracellular subendothelial proteoglycan matrix that their rapid freeze etching technique preserves (see Addendum). Using a heterogeneous fiber matrix theory, which includes proteoglycan and collagen components, the model predicts that the Darcy permeability Kp and macromolecular diffusivity D of the subendothelial intima is two orders of magnitude larger than the corresponding values measured in the media, and supports the observations in Lark et al. [24] that the proteoglycan structure of the intima differs greatly from that of the media. Numerical results show that convection parallel to the endothelium is a very significant transport mechanism for macromolecules in the intima in a large region of roughly 200 microns diameter surrounding the leaky cleft. The predictions of the new model for the early-time spread of the advancing convective-diffusive front from the leakage spots in the intima are in close agreement with our experimental measurements for the growth of HRP spots in [20]. The regions of high concentration surrounding the leaky cell, however, are much more limited and cover an area that is typically equivalent to 20 cells. This prediction is consistent with the recent measurements of Truskey et al. for LDL spot size in rabbit aorta [21] and the hypothesis advanced in [19] that there is a colocalization of subendothelial liposome growth and cellular level leakage. Finally, comparison of predicted and experimentally-measured average LDL concentration in leakage spots strongly suggests that there is significant local molecular sieving at the interface between the fenestral openings in the internal elastic lamina and the media.

Animals↗
PubMed1994

Incorporation of excess wild-type and mutant tRNA(3Lys) into human immunodeficiency virus type 1.

Human immunodeficiency virus (HIV) particles produced in COS-7 cells transfected with HIV type 1 (HIV-1) proviral DNA contain 8 molecules of tRNA(3Lys) per 2 molecules of genomic RNA and 12 molecules of tRNA1,2Lys per 2 molecules of genomic RNA. When COS-7 cells are transfected with a plasmid containing both HIV-1 proviral DNA and a human tRNA3Lys gene, there is a large increase in the amount of cytoplasmic tRNA3Lys per microgram of total cellular RNA, and the tRNA3Lys content in the virus increases from 8 to 17 molecules per 2 molecules of genomic RNA. However, the total number of tRNALys molecules per 2 molecules of genomic RNA remains constant at 20; i.e., the viral tRNA1,2Lys content decreases from 12 to 3 molecules per 2 molecules of genomic RNA. All detectable tRNA3Lys is aminoacylated in the cytoplasm of infected cells and deacylated in the virus. When COS-7 cells are transfected with a plasmid containing both HIV-1 proviral DNA and a mutant amber suppressor tRNA3Lys gene (in which the anticodon is changed from TTT to CTA), there is also a large increase in the relative concentration of cytoplasmic tRNA3Lys, and the tRNA3Lys content in the virus increases from 8 to 15 molecules per 2 molecules of genomic RNA, with a decrease in viral tRNA1,2Lys from 12 to 5 molecules per 2 molecules of genomic RNA. Thus, the total number of molecules of tRNALys in the virion remains at 20. The alteration of the anticodon has little effect on the viral packaging of this mutant tRNA in spite of the fact that it no longer contains the modified base mcm 5s2U at position 34, and its ability to be aminoacylated is significantly impaired compared with that of wild-type tRNA3Lys. Viral particles which have incorporated either excess wild-type tRNA3Lys or mutant suppressor tRNA3Lys show no differences in viral infectivity compared with wild-type HIV-1.

Animals↗
PubMed1994

Phase II study of hepatic arterial floxuridine, leucovorin, and dexamethasone for unresectable liver metastases from colorectal carcinoma.

PURPOSE: To determine the toxicity, response rate, and survival of a regimen of hepatic arterial floxuridine (FUDR) with leucovorin (LV) and dexamethasone (Dec) for the treatment of unresectable hepatic metastases from colorectal carcinoma. PATIENTS AND METHODS: Sixty-two patients with hepatic metastases (33 previously untreated with chemotherapy) were treated with FUDR (0.30 mg/kg/d) and LV (15 mg/m2/d) and Dec (20 mg total dose) as a 14-day hepatic arterial infusion via an implantable pump alternating with 2 weeks of saline. RESULTS: The complete response (CR) plus partial response (PR) rate was 78% in previously untreated patients, with a median survival duration of 24.8 months; 1- and 2-year survival rates were 91% and 57%, respectively. In the previously treated group, the response rate was 52%, with a median survival duration of 13.5 months. Only 3% of patients (two of 62) developed biliary sclerosis; this was significantly lower than the 21% biliary sclerosis rate observed in our previous trial of hepatic arterial FUDR and LV without Dec (P = .002). CONCLUSION: The addition of Dec to hepatic arterial FUDR and LV reduces biliary toxicity while maintaining an excellent response rate and survival. We recommend that this treatment be studied further.

Adult↗
PubMed1994

Suppression in gonadotropes of gonadotropin-releasing hormone-stimulated follicle-stimulating hormone release by the gonadal- and neurosteroid 3 alpha-hydroxy-4-pregnen-20-one involves cytosolic calcium.

The gonadal- and neurosteroid 3 alpha-hydroxy-4-pregnen-20-one (3 alpha HP) suppresses FSH release in cultures of anterior pituitary cells. In a previous report, we showed that this suppression is achieved at least in part by an interaction at the plasma membrane level. We undertook to examine the possible interaction of 3 alpha HP at the level of intracellular Ca2+. Anterior pituitary cells from adult randomly cycling female rats were treated for 4 h with 10 nM GnRH and 0.1 nM 3 alpha HP with or without protein kinase C activator (SC10), antagonist (H-7), intracellular Ca2+ chelator (TMB-8), and intracellular Ca2+ mobilizer (glutamate), and with or without EGTA and Ca2+ in the medium. FSH content in media and cells was determined by RIA. The protein kinase C (PKC) activator, SC10, increased basal levels of secreted FSH. 3 alpha HP suppressed (P < 0.05) SC10-stimulated basal FSH release. The PKC inhibitor, H7, decreased GnRH-induced FSH release; FSH was further suppressed (P < 0.05) by 3 alpha HP in the presence of H7. These results were interpreted to indicate that 3 alpha HP may act in part at the level of PKC and also at another site(s). The intracellular Ca2+ chelator, TMB-8, suppressed released and cellular GnRH-stimulated FSH to the same extent as 3 alpha HP; FSH was not further decreased by 3 alpha HP in the presence of TMB-8. 3 alpha HP suppressed glutamate-stimulated FSH release in Ca(2+)-free medium (P < 0.01). Moreover, GnRH-induced release of FSH was suppressed to the same degree by 10(-10) M 3 alpha HP as by 10(-4) M EGTA. In pituitary cell suspensions, the GnRH-induced [Ca2+]i elevations were significantly (P < 0.05) attenuated by 3 alpha HP. From these and previous results, a model is proposed for the action of 3 alpha HP. The model suggests that 3 alpha HP may interact with gonadotropes at the level of the PKC cell signaling pathway and intracellular Ca2+ mobilization, in addition to the plasma membrane/calcium channel. The interaction effects a decrease in intracellular Ca2+, leading to decreases in FSH release from those pituitary gonadotropes that are responsible for FSH. The consistent decrease in total FSH (released plus cellular content) by 3 alpha HP suggests that this neurosteroid may also suppress FSH synthesis.

20-alpha-Dihydroprogesterone↗
PubMed1994

Molecular cloning and characterization of a novel liver-specific transport protein.

Monoclonal antibodies that specifically recognize a membrane component located on the sinusoidal domain of the hepatocyte have been used to screen a rat liver cDNA expression library and a clone encoding a novel transporter (NLT) protein has been identified. Analysis of the deduced 535 amino acid protein sequence indicates that it is unique, but shares the twelve-transmembrane domain hydrophathicity profile as well as the presence of transporter-specific amino acid motifs with bacterial and mammalian transporters. Since overall homology of NLT to known transporter genes is low (20-25% identity) it may represent a new subgroup within the transporter family of proteins. The NLT was characterized further with respect to its tissue distribution and its expression during liver development. A 2.1 kb transcript has been found in liver and at lower levels in kidney, but not in several other tissues tested. Studies on the developing liver indicate that NLT transcripts are present at a very low level from 19 through 21 gestation days with a 4- to 5-fold increase within two weeks after birth. Overall, we have cloned a novel transporter that is preferentially expressed in liver, is located on the sinusoidal domain of the plasma membrane and represents a marker for the late stage of liver development.

Amino Acid Sequence↗
PubMed1994

Combined antileukemic activity of pIXY 321 and Ara-C against human acute myeloid leukemia cells.

Prolonged administration of conventional (100 mg/m2/day) or low dose Ara-C (20 mg/m2/day) has been associated with significant clinical antileukemic effects in AML and myelodysplastic syndromes. These doses and schedules of Ara-C yield plasma Ara-C concentrations in the range of 10 to 100 nM. Utilizing concentrations and a schedule of Ara-C treatment, representative of Ara-C exposures in these clinical situations, we performed in vitro studies to examine the effects of co-treatment with pIXY 321 on Ara-C induced apoptosis and Ara-C-mediated colony growth inhibition of human myeloid leukemia HL-60 cells. Significantly greater internucleosomal DNA fragmentation, higher percentage of morphologically recognizable apoptotic cells and increased colony growth inhibition were observed following treatment with 100 versus 10 nM Ara-C for 5 days. Simultaneous exposure to 10 ng/ml pIXY 321 resulted in significantly increased colony growth inhibition as well as DNA fragmentation and apoptosis due to 10 nM but not 100 nM Ara-C. These concentrations of Ara-C inhibited c-myc and did not induce c-jun mRNA expression. These effects of Ara-C on c-myc and c-jun expressions were not influenced by co-treatment with pIXY 321. Neither treatment with pIXY 321 or Ara-C alone, nor co-treatment with pIXY 321 and Ara-C, significantly altered the intracellular p26BCL-2 levels in HL-60 cells. These results indicate that co-treatment with pIXY 321 significantly increases low dose Ara-C-induced apoptosis and thereby its antileukemic activity.

Acute Disease↗
PubMed1994

Reverse transcriptase is an important factor for the primer tRNA selection in HIV-1.

During assembly, HIV-1 selectively packages tRNA(Lys3), the primer tRNA for reverse transcriptase (RT). Because of tRNA(Lys3)'s ability to interact with RT, RT may be the viral protein which binds to primer tRNA and carries it into the virus. We have tested this hypothesis by measuring the amount of tRNA(Lys3) incorporated into wild type and RT(-) virus, and have also measured the tRNA tightly associated with the RNA genome, a characteristic of primer tRNA. We find that in RT(-) HIV-1, primer tRNA(Lys3) is reduced approximately 10 fold compared to wild type virus (which contains 8 molecules tRNA(Lys3)/virus), and the tRNA found tightly associated with the RNA genome is also greatly reduced in these mutant virus.

Cell Line↗
PubMed1994

[Serological investigation on intrafamilial transmission of HCV infection].

To clarify the intrafamilial transmission of HCV infection, the antibody to HCV was assayed in 124 serum samples from the family members of 60 HCV-Ab (+) index cases (group C), and compared with that from 83 family members of 40 HCV-Ab (-) index patients with hepatitis B (group B), Nine of 124, including 2 parents, 6 spouse and 1 granddaughter, were positive for anti-HCV. The prevalence of anti-HCV was 7.3% (9/124) in total, and 1.85% (2/108) in the subjects who had no history of blood donation. None of 83 was positive for anti-HCV in group B. On the other hand, the prevalence of HBV infection was 25.33% in the group of HCV infection only, and 40.91% in the group with HBV/HCV double-infection or HBV infection. It indicates that the risk of HBV intrafamilial transmission is higher than that of HCV, and the risk of transmission of HCV from mother to infant may be lower than that of sexual transmission.

Adolescent↗
PubMed1994

High levels of p26BCL-2 oncoprotein retard taxol-induced apoptosis in human pre-B leukemia cells.

In human leukemic cells clinically relevant concentrations of taxol have been demonstrated to induce the biochemical and morphologic hallmarks of apoptosis (Leukemia 1993;7:563-568). Since overexpression of the bcl-2 gene has been reported to retard apoptosis due to a variety of anticancer agents, we examined and compared taxol-induced intracellular microtubular bundling and apoptosis in pre-B human leukemia 697 cells and their counterparts which have been transfected with and overexpress cDNA derived from the bcl-2 gene. Treatment with 0.1 or 1.0 mumol/l taxol for 24 h resulted in internucleosomal DNA fragmentation and morphologic features of apoptosis in 697 cells, but not in 697/BCL-2 cells. However, indirect immunofluorescent staining with anti-tubulin antibody revealed that taxol treatment produces stable microtubule bundles resistant to calcium-mediated disassembly in 697, as well as 697/BCL-2 cells. In addition, taxol-induced microtubule bundling was associated with a marked accumulation of the two cell types in the G2/M phase of the cell cycle. Following exposure to taxol, when 697 cells were washed and kept in drug-free medium, they showed rapid onset of apoptosis followed by loss of cell viability and a decline in cell numbers. In contrast, identically treated 697/BCL-2 cells kept in drug-free medium remained in a growth arrested state, but showed little evidence of apoptosis for up to 4 days. They eventually demonstrated features of apoptotic cell death and loss of viability between 5 and 7 days. This was not accompanied by a decrease in p26BCL-2 levels. Anti-phosphotyrosine or anti-MAP kinase immunoblot analyses of proteins isolated from taxol-treated 697 and 697/BCL-2 cells failed to show any difference in tyrosine phosphorylation of cellular proteins. Therefore, our findings indicate that in 697/BCL-2 cells, high levels of p26BCL-2 significantly delay taxol-induced endonucleolytic internucleosomal DNA fragmentation and apoptosis, but do not affect taxol-induced microtubule bundling or cell cycle growth arrest. The delayed onset of taxol-induced DNA fragmentation and apoptosis in 697/BCL-2 cells without down-regulation of p26BCL-2 levels suggests that an alternative mechanism of taxol-mediated apoptosis might be triggered which is unimpeded by high p26BCL-2 levels, or taxol-induced prolongation of mitotic arrest may lead to the inactivation or inhibition of that mechanism by which p26BCL-2 is able to block apoptosis.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Oral transmucosal back permeation of alfentanil in dogs--a novel method to determine blood alfentanil concentration.

This study explores a novel noninvasive method for monitoring blood alfentanil concentrations using a dog model. Alfentanil which "back" permeated across the oral mucosa from the systemic circulation was collected from the oral mucosal surface and quantitated. The levels of the "back" permeated alfentanil were found to closely reflect real time serum alfentanil concentrations. With further work, this finding may lead to a novel noninvasive method for monitoring real time serum alfentanil concentrations in its clinical applications.

Alfentanil↗
PubMed1994

The mitochondrial DNA mutation at position 11778 in Chinese families with Leber's hereditary optic neuropathy.

We amplified the 340 bp of mitochondrial DNA (mtDNA) by PCR including the recognized sequence of restriction enzyme of SfaN I. After amplification and digestion of SfaN I, two bands of 190 bp and 150 bp appeared in the mtDNA of four normal individuals but only one band of 340 bp appeared in the mtDNA with the mutation of G to A at the site of the nucleotide 11778 because such mutation destroyed the recognized sequence of SfaN I. We studied the mtDNAs of the patients with Leber's hereditary optic neuropathy from 19 Chinese families and their maternal relatives as well as the normal individuals i. e. the husbands of the female members of the pedigrees. The results show that 66.7% of the patients (30/45) and 54.7% of the maternal relatives (29/53) have such a mutation, while no such a mutation exists in the four normal individuals. So, we conclude that the mutation of mitochondrial DNA at position 11,778 is also a major cause of LHON in China.

Asian People↗
PubMed1994

[Effects of fibronectin on cytodifferentiation (T56) of human squamous cell carcinoma of tongue].

Fibronectin (FN) are large glycoproteins that have been implicated in a wide variety of cellular properties, including cell adhesion, morphology, cytoskeletal organization, migration, differentiation, and oncogenic transformation. T56 cells were treated with 20, 50, and 100 micrograms/ml of FN for 48 h, and the changes in cells were analysed qualitatively and quantitatively with the methods of transmission electron microscopy, enzyme cytochemistry, and cell electrophoresis, etc. The studies were made to test the effects of FN on T56 cells in biological behaviour in terms of cell growth, multiplication, cell metabolism, cell electrophoresis and surface morphology. The results indicated that FN could partially restore T56 cell normal epidermic cell's phenotype, inhibit cell mitosis, increase contact of cells, decrease the number of microvilli and ruffles, and promote cell oxybiotic metabolism. These results suggest that FN might relate in many aspects to the biological behaviour of T56 cell and could affect changes in the behaviour.

Carcinoma, Squamous Cell↗
PubMed1994

[Herpes zoster keratoendotheliitis].

Herpes zoster keratoendotheliitis is related to autoimmunity or herpes zoster virus infection. It is characterised by K.P. and interstitial edema. The disease responds well to the administration of steroids and a good result is often achieved.

Adrenal Cortex Hormones↗
PubMed1994

[Synchronous analysis of multi-channel spectrum for human resonance cavity].

The synchronous analysis of multichannel spectrum were used to determine the regulars, conditions and characters of the resonance when subjects pronounced. 140 subjects were selected for test and 1040 pieces of sound sample were collected, then the analysis of different parts (mouth, throat, head and chest) was done. The results of the analysis of variance showed that there was much difference among the various professional workers, different places of articulation, and patients with voice disorders in spectrum analysis (P < 0.001). Each part of resonance frequencies was put forward of pronouncing system. High frequency resonance comes from head and pharynx (above 2000 Hz high resonance cavity), and low frequency resonance comes from chest and larynx (less than 2000 Hz resonance cavity). We suggest that there are six degrees of clinical objective classification of the pathologic hoarseness.

Female↗