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Biomedical subjects

L Bai

Publications and source records attributed to L Bai.

At least 55 records · Page 3Linked to original sources

[Synovial chondromatosis: clinical analysis of 13 cases].

OBJECTIVE: To study the diagnosis and treatment of synovial chondromatosis. METHOD: 13 cases of synovial chondromatosis were studied by pathological observation, X-ray examination and clinical research. RESULTS: Intermittent joint pain, swelling, limited motion, joint snapping or rubbing were found, sometimes with joint interlocking and movable mass in the joint. X-ray showed fewer loose bodies than the actual ones in the joint. Rough surface, congestion and thickening of synovial membrane at the lesion were found during the operation. Proliferation of blood vessels, accumulation of lymphocytes and proliferation of synovial superficial cells and fibrous tissue were observed under the microscope. The loose body consisted of many tubercles microscopically. CONCLUSIONS: The combination of clinical observation, X-ray examination and pathological diagnosis is essential to the diagnosis of synovial chondromatosis. Excision of loose body and synovial membrane may lead to satisfying results.

Adolescent↗

[Transposition of Tn5096 in a agricultural antibiotic 120 roducer Streptomyces hygrospinocus var. beijingensis RF220].

No transformant was obtained when pCZA168(bla, tsr, Tn5096, ColEI rep. Strep repts) was used to transform S. hygropinocus RF220. pIJ702 isolated from S. hygroscopicus N103 was transformed into RF220 at a low frequency. pIJ702 plasmid was cured in RF220 transformant and it was re-transformed into its cured FR220 strain, but the transformation frequency was not increased significantly, suggesting that restriction-modification system in FR220 was existent and complicated. Four transformants containing pCZA168 were obtained, when the RF220 strain was grown in medium with ampicillin, glycine and the protoplast was stored at -70 degrees C. Restriction analysis of plasmid from transformants indicated that the DNA fragment from E. coli in pCZA168 was deleted. With transposition of Tn5096, two mutants blocked in antibiotic biosynthesis of 120 and some mutants with variation in antibiotic level were obtained, this showed that the Tn5096 transposed in different positions of chromosomal DNA in RF220 and resulted in the production of 120 in different level.

Anti-Bacterial Agents↗

Molecular cloning and characterization of the rat NHE-2 gene promoter.

To understand the molecular mechanisms underlying NHE-2 regulation in the mammalian kidney and intestine, we cloned and sequenced 5.6 kb of the 5'-flanking region of the rat NHE-2 gene. DNA sequence analysis revealed multiple putative cis-acting regulatory elements including SP1, CK, NFY-CBF, Tant, GCN4, and one progesterone and several retinoic acid response elements. The upstream sequence lacked TATA and CAAT boxes, but contained a high G/C rich region within the first 300 bp. A single transcriptional initiation site was identified by primer extension in rat kidney and small intestine, approximately 103 bp upstream of the previously identified 5'-end of the rat NHE-2 cDNA. Various regions of the promoter (from [-]5567 to [+]105 bp) were tested for their ability to drive expression of the luciferase reporter gene in transiently transfected murine Inner Medullary Collecting Duct (mIMCD-3) cells. Results demonstrated that [-]289, [-]1271 and [-]2630 bp constructs showed promoter activity that was significantly higher than the negative control construct (20-fold). These results also demonstrated that basal cis-acting elements are contained within [-]289 bp of the transcriptional start site. However, the functional activity of the [-]5567 bp construct was not significantly different from the negative control, suggesting that a negative regulatory element may be present between [-]2630 and [-]5567 bp of the promoter region.

Animals↗

The substrate recognition domain in the Na+/dicarboxylate and Na+/sulfate cotransporters is located in the carboxy-terminal portion of the protein.

The Na+/dicarboxylate cotransporter, NaDC-1, and the Na+/sulfate cotransporter, NaSi-1, share 43% sequence identity, but they exhibit no overlap in substrate specificity. A functional chimera, SiDC-4, was prepared from NaDC-1 and NaSi-1 by homologous recombination and expressed in Xenopus oocytes. SiDC-4 contains putative transmembrane domains 1-4 of NaSi-1 (amino acids 1-139) and putative transmembrane domains 5-11 of NaDC-1 (amino acids 141-593). SiDC-4 retains the substrate specificity of NaDC-1, which suggests that the substrate recognition domain is found in the carboxy-terminal portion of the protein, past amino acid 141. However, residues that affect substrate affinity and inhibition by furosemide and flufenamate are found in the amino terminal third of the protein. The cation binding properties of SiDC-4, including a stimulation of transport by lithium, differed from both parental transporters, suggesting that cation binding is determined by interactions between the amino- and carboxy-terminal portions of the protein. We conclude that the substrate recognition site of NaDC-1 and NaSi-1 is found in the carboxy-terminal portion of the protein, past amino acid 141, but residues in the amino terminus can affect substrate affinity, inhibitor sensitivity, and cation selectivity.

Animals↗

Mechanisms responsible for resistance of sublines derived from leukemia cell lines to an antitumor agent 9-beta-D-arabinofuranosyl-2-fluoroadenine.

An agent 9-beta-D-arabinofuranosyl-2-fluoroadenine (2-F-Ara-A) is a main metabolite of fludarabine, a fluorinated purine analogue with antitumor activity in lymphoproliferative malignancies. In this study, the mechanism responsible for the resistance of cancer cells to fludarabine was examined using the 2-F-Ara-A-resistant sublines JOK-1/F-Ara-A and L1210/F-Ara-A from a human hairy leukemic cell line (JOK-1) and a mouse leukemic cell line (L1210) respectively, which were established by continuous treatment of the parental cell lines with 2-F-AraA. JOK-1/F-Ara-A and L1210/F-Ara-A cells were more than 55 and 29 times more resistant to 2-F-Ara-A than were their parent cell lines, and showed a high cross-resistance to 1-beta-D-arabinofuranosylcytosine but not to doxorubicin or vincristine. These resistant sublines intracellularly accumulated almost the same amount of 2-F-Ara-A as did their parent cell lines. However, the amount of 2-F-Ara-ATP, a cytotoxic metabolite of 2-F-Ara-A, decreased by 2.6% (JOK-1/F-Ara-A C3), 6% (L1210/F-Ara-A C1) and 3.7% (L1210/F-Ara-A C7) relative to the levels in the parent cell lines. Enzymatically, these resistant cells hardly activated deoxycytidine (dCyd) and 2-F-Ara-A. In addition, the abilities to phosphorylate deoxyadenosine and deoxyguanosine were also decreased in the resistant cells in comparison with the parent cells. These findings suggest that the deficiency in activity of dCyd kinase may contribute to the resistance of 2-F-Ara-A.

Animals↗

Macronodular multi-organs tuberculoma: CT and MR appearances.

The case of a 21-year-old woman presenting with macronodular multi-organs tuberculoma is reported. She was examined for pulmonary tuberculosis on a chest X-ray film in January, 1995, and admitted with a cough, anorexia, and abdominal pain in July, 1996. Computed tomography revealed multiple calcified nodules with peripheral hypodense areas in the brain, and calcified hypodense masses in the liver and spleen. Magnetic resonance (MR) imaging showed hypointense masses in the liver and spleen on T1-weighted spin echo images and a hypointense mass with a hyperintense area on T2-weighted spin echo images. On contrast-enhanced dynamic MR images, the liver and spleen masses were unenhanced and hypointense with slight rim enhancement. T2-weighted spin echo images showed a round hypointense nodule in the right kidney and hydronephrosis and enlargement in the left kidney. Antituberculous treatment was started with a gradual improvement in her signs and symptoms. Her temperature became normal. However, she was systemically treated with antituberculous chemotherapy 10 months later, her condition worsened again. She died from increased intracranial pressure in August, 1997.

Adult↗

Effect of cholesterol/phospholipid ratio on stimulatory GTP-binding protein function.

The effect of different cholesterol/phospholipid (C/P) ratios on the coupling function between stimulatory GTP-binding protein(Gs) and adenylyl cyclase (AC) in proteoliposomes, and its relationship to the conformational change of Gs were investigated. The results showed that Gs activities of both binding GTP gamma S and stimulating adenylyl cyclase were the highest in proteoliposomes with a proper content of cholesterol similar to physiological situation while the lowest with higher cholesterol content similar to pathological situation. In addition, the conformational change of Gs in proteoliposomes was also detected by steady-state and nanosecond time-resolved fluorescence using acrylodan as a probe. It is suggested that a proper C/P ratio similar to physiological situation regulates the function of Gs by inducing a change in the physical state of lipid bilayer, which would favor the formation of a suitable conformation of Gs with higher activities of both binding GTP and stimulating adenylyl cyclase. But if C/P ratio is higher, such as in pathological situation, this is unfavorable for motion of Gs in membrane, which results in inhibition of Gs function significantly.

Animals↗

[Scavenging action of shengmaiyin decoction on hydroxyl radical].

A study has been made on the scavenging action of Shengmaiyin Decoction and its ingredients Radix Ginseng, Radix Ophiopogonis and Fructus Schisandrae on hydroxyl radical, as well as on the relationship between the decoction and its ingredients using ESR spin-trapping. The results indicate that the decoction is better in antioxidation than its ingredients.

Drug Combinations↗

[Studies on genes associated with biologic behavior in human lung cancer].

OBJECTIVE: To study alteration of several genes in the process of primary lung cancer. METHODS: A series of 59 lung cancer specimens were analyzed for p53, myc oncogene family and mdrl gene by DNA/PCR sequencing, immunohistochemistry and RT-PCR methods. RESULTS: p53 mutation or/and protein accumulation were found in 37 of 57(65%) cases. Overexpression of myc family oncogenes and mdr1 gene were 27/46 (59%) and 15/48 (31%), respectively. The results also showed that there was no significant correlation between p53 alteration and tumor size, metastasis, stage and relapse, but there was a significant correlation between overexpression of myc family oncogene and these factors. Overexpression of mdrl gene was detected in NSCLC, especially in adenocarcinoma, and was not associated with metastasis and stage of lung cancer. It was also found that aberration of both p53 and myc family oncogenes occurred in 19/30(63%) cases; the relapse rate was 76%. Both overexpression of mdrl and myc gene was 62%; the relapse rate was 83%. CONCLUSION: p53, myc and mdrl genes in cooperation may be involved in the process of lung cancer, but prognostic determinant is myc gene overexpression.

Adenocarcinoma↗

Isolation of a gene encoding nodulin-like intrinsic protein of Escherichia coli.

Members of the membrane intrinsic protein (MIP) family are expressed in various organisms including plants, insects, and vertebrates. E. coli is known to have a MIP member gene, glycerol facilitator (G1pF). Here we report the isolation of E. coli gene encoding BniP, bacterial nodulin-like intrinsic protein. BniP encodes a 231 amino acid, 24 kDa protein with 42% amino acid identity to Nod26, 38% amino acid identity to AQP1, and 29% amino acid identity to G1pF. Analysis of deduced amino acid sequence predicted a hydrophobic protein with six membrane-spanning domains. Expression of BniP in Xenopus oocytes induced slight increase in osmotic water permeability, but not glycerol or ion permeability. Our results showed that BniP is a new member of the MIP channel-forming proteins of E. coli.

Amino Acid Sequence↗

Expression cloning of NaDC-2, an intestinal Na(+)- or Li(+)-dependent dicarboxylate transporter.

A cDNA coding for a Na(+)-dicarboxylate cotransporter from Xenopus laevis intestine, NaDC-2, was isolated by functional expression cloning in Xenopus oocytes. NaDC-2 encodes a 622-residue polypeptide with a predicted mass of 68.6 kDa. The sequence and secondary structure of NaDC-2 are related to the mammalian renal Na(+)-dicarboxylate and Na(+)-sulfate cotransporters. NaDC-2 mRNA is expressed only in the intestine. Oocytes injected with NaDC-2 cRNA exhibit increased transport of succinate, citrate, and glutarate. Transport of succinate by NaDC-2 is stimulated by Na+ or Li+, with Michaelis-Menten constant values for succinate of 0.3 mM (in Na+) and 0.7 mM (in Li+). Na+ and Li+ activation curves show sigmoid kinetics, with Hill coefficients of 1.4 (nNa) and 1.7 (nLi), indicating that multiple cations are involved in the transport of succinate. The transport of succinate by NaDC-2 is insensitive to pH, whereas the transport of citrate is inhibited at high pH. The differences in functional properties between NaDC-2 and the structurally related Na(+)-dicarboxylate cotransporters NaDC-1 and hNaDC-1 will form the basis of detailed structure-function studies.

Amino Acid Sequence↗

[Relationship of mdr1 gene expression and multidrug resistance of primary lung cancer].

OBJECTIVE: To evaluate the expression of mdr1 gene in various type of primary lung cancer. METHOD: A serious of 48 resected primary lung cancer tissues from 5 post-chemotherapy and 43 untreated patients and 33 adjacent normal lung tissues were analyzed for mdr1 gene by RT-PCR method. RESULTS: Fifteen of 48 tumor tissues were found to have overexpression of mdr1 gene, comprising 6 of 12 adenocarcinomas, 7 of 22 squamous cell carcinomas, 1 of 2 sarcocarcinomas, 1 of 12 small cell carcinomas. Of 5 post-chemotherapy specimens, only one case showed positive. In addition, 3 of 33 adjacent normal tissues also showed mdr1-positive. Overexpression of mdr1 gene did not be associated with tumor size, metastasis and stage of lung cancer. The relapse rate with mdr1-positive cases was higher (80%) than that with mdr1-negative (58%) by one year follow-up of these patients. CONCLUSION: Overexpression of mdr1 gene can be detected in untreated primary lung cancer, specially in non-small cell lung cancer and may be regarded as one poorly prognostic marker.

Adenocarcinoma↗

Ketamine-induced peripheral analgesia in rats.

AIM: To examine whether ketamine may directly act at peripheral nociceptors to produce analgesia. METHODS: Wistar rats were anesthetized with urethane. As a nociceptive flexion reflex (FR), C responses from the posterior biceps semitendinosus (PBST) muscle was evoked by electrical stimulation (2 ms, 80 V, 2-3 pulses, 0.5 Hz) via a pair of stainless steel needles inserted subcutaneously applied to the two toes of ipsilateral hindpw. RESULTS: Subcutaneous injection of ketamine (36 mmol.L-1, 5 microL) into the ipsilateral hindpaw produced an inhibition of C responses. At 9 min after application of ketamine, injection of naloxone (1%, 5 microL) into the same area annulled ketamine-induced inhibition. CONCLUSION: Ketamine as a dissociate anesthetic acts on peripheral nociceptors to produce analgesia, which is related to activity of peripheral opioid receptors.

Analgesics↗

Relationship of p53 alteration and myc family gene overexpression with the clinical characteristics of lung cancer.

OBJECTIVE: To evaluate the relationship of p53 alteration and myc family gene overexpression with the clinical characteristics of lung cancer. METHODS: A series of 59 resected primary lung cancer specimens was analyzed for p53 gene by DNA/PCR sequencing and immunohistochemistry technique, and for myc family genes by RT-PCR methods. RESULTS: Thirty-seven of 57 tumors were found to have p53 mutations or/and p53 protein accumulation. The presence of p53 alteration was not related to tumor size, lymph node metastasis, stage and relapse. Forty-seven cases were analyzed for myc family genes. The results showed that there was a positive correlation between unregulative expression of myc genes and the above mentioned clinical parameters. Our finding also showed that 19 of 30 cases (63%) with p53 alteration had myc gene overexpression which occurred in 63% and 76% cases with stage III and relapse, respectively, which was higher than 27% and 22% with p53 alteration but no myc gene overexpression and 50% and 71% with p53 negative but myc gene overexpression. CONCLUSIONS: p53 alteration is a vital genetic event in the earlier stage of lung carcinogenesis, but not a prognostic marker. myc family genes overexpression may be regarded as one of the independent prognostic determinants in lung cancer. The cooperation between p53 alteration and myc gene overexpression may occur during progression of lung cancer, but prognostic determinant is myc gene overexpression.

Adenocarcinoma↗

Structure of aquaporin-2 vasopressin water channel.

Aquaporin-2 (AQP-2) is a vasopressin-regulated water channel in the kidney collecting duct. AQP-2 is selectively permeable to water molecule and is translocated between the apical membrane and subapical endosomes in response to vasopressin. To investigate the localization and structure of the aqueous pathway of the AQP-2 water channel, a series of site-directed mutants was constructed and functionally analyzed. Insertion of N-glycosylation reporter sequence into each hydrophilic loop (HL) indicated that AQP-2 has a six-membrane spanning topology and that insertional mutations in HL-2 or HL-5 do not alter water channel function. Mercury-sensitive site of AQP-2 is located near the second asparagine-proline-alanine (NPA) domain at cysteine 181, but not near the first NPA domain. Replacement of HL-3 or HL-4 with the corresponding part of Escherichia coli glycerol facilitator abolished water channel function without changing plasma membrane expression of the channel protein. Introduction of cysteine residues in His-122, Asn-123, Gly-154, Asp-155, or Asn-156 induced partial mercury sensitivity, and point mutations in asparagine 123 significantly altered water permeability. Our results implicate that the structure of AQP-2 is different from models previously proposed for AQP-1 and that HL-3 and HL-4 are closely located to the aqueous pathway.

Amino Acid Sequence↗

Cloning and characterization of the beta subunit of human proximal sequence element-binding transcription factor and its involvement in transcription of small nuclear RNA genes by RNA polymerases II and III.

The proximal sequence element (PSE)-binding transcription factor (PTF), which binds the PSE of both RNA polymerase II- and RNA polymerase III-transcribed mammalian small nuclear RNA (snRNA) genes, is essential for their transcription. We previously reported the purification of human PTF, a complex of four subunits, and the molecular cloning and characterization of PTF gamma and delta subunits. Here we describe the isolation and expression of a cDNA encoding PTF beta, as well as functional studies using anti-PTF beta antibodies. Native PTF beta, in either protein fractions or a PTF-Oct-1-DNA complex, can be recognized by polyclonal antibodies raised against recombinant PTF beta. Immunodepletion studies show that PTF beta is required for transcription of both classes of snRNA genes in vitro. In addition, immunoprecipitation analyses demonstrate that substantial and similar molar amounts of TATA-binding protein (TBP) and TFIIIB90 can weakly associate with PTF at low salt conditions, but this association is dramatically reduced at high salt concentrations. Along with our previous demonstration of both physical interactions between PTF gamma/PTF delta and TBP and the involvement of TFIIIB90 in the transcription of class III snRNA genes, these results are consistent with the notion that a TBP-containing complex related to TFIIIB is required for the transcription of class III snRNA genes, and acts through weak interaction with the four-subunit PTF.

Amino Acid Sequence↗

[Data analysis on the causes of death through disease surveillance program in Gansu province in the early 1990's].

In order to observe the changes of the causes of death among the residents in Gansu, mortality and years of porential life lost (YPLL) are used in this article to analyse the data of causes of death in 1990-1994. Data indicates that the average mortality of residents was 591.98 per 100,000. The main sequence were as below: respiratory diseases, cardiorasculor and cerebrovascalar diseases, neoplasms, injuries and pediatric diseases. Chronic diseases take up 74.4% of an mortalities. Average YPLL was 55.84/1000. YPLL sequence was as follows: injuries, neoplasms, respiratory system diseases, infectious diseases, cardiorascular diseases.

Accidents↗