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Biomedical subjects

B Yao

Publications and source records attributed to B Yao.

At least 55 records · Page 3Linked to original sources

Studies on the in vitro cultivation of Babesia from buffaloes.

This paper summarizes a recent study on the in vitro cultivation of Babesia from buffaloes. Buffalo Babesia parasites were cultured many times by the microaerophilous stationary phase (MASP) method of Levy and Ristic (1980) with some modifications. The culture-derived Babesia organisms were similar to forms seen in the blood of infected buffaloes and the pathogenicity of these organisms was unchanged. Factors influencing the in vitro cultivation are discussed in detail.

Animals↗

Studies on the pathogenicity of Babesia bovis in water buffaloes after cryopreservation and resuscitation.

Packed erythrocytes infected with Babesia bovis were mixed with an equal volume of 16% dimethyl sulphoxide (DMSO) in Alsever's solution and dispensed into 1.5 or 5 ml cryotubes. The vials were kept in liquid nitrogen (-196 degrees C) for 26, 78, 142 or 149 days. The samples were removed from the liquid nitrogen container and rapidly thawed in a 40 degrees C water bath. The thawed blood successfully infected splenectomised buffalo calves by injection via subcutaneous or intravenous or via intravenous and subcutaneous routes. The parasites, typical B. bovis, were discovered in red blood cells 5, 8 or 9 days after inoculation. The highest percentage of parasitised erythrocytes (PPE) was 15%. The babesiosis resulting from cryopreserved parasites was the same as that resulting from fresh parasites inoculated by ticks. Typical clinical signs were found, such as continuous fever (the highest temperature was 41.3 degrees C), anaemia, icterus and haemoglobinuria. Infected calves, which were not treated, died. Cryopreservation is a simple and reliable method for longterm preservation of B. bovis of water buffaloes.

Animals↗

[Inhibition of peripheral blood T cell proliferation by dexamethasone in steroid-resistance asthma].

We investigated the pathogenesis of steroid-resistance (SR). The inhibition of phyto-hemagglutininum-induced T lymphocyte proliferation by dexamethasone (Dex) was investigated by lymphocyte proliferation assay. Plasma cortisol concentration was measured by radioimmune lectrophoresis autoradiography kit. The inhibition effects of Dex (10(-7) mol/L) on the proliferation of lymphocytes from SR asthmatics were significantly less than those from steroid-sensitive (SS) asthmatics (P < 0.05). Plasma cortisol concentrations of SR asthmatics were significantly lower than those of normal subjects (P < 0.01) and SS asthmatics (P < 0.05). There was no correlation between the degree of inhibition by Dex (10(-7) mol/L of SR, SS asthmatics of proliferation of T lymphocytes and plasma cortisol concentration. T lymphocytes from SR asthmatics were insensitive to Dex. Plasma cortisol concentration from SR asthmatics were significantly lower than those of SS asthmatics, that may be due to the large dose of glucocorticoids given in long time.

Adult↗

Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis.

The induction of programmed cell death, or apoptosis, involves activation of a signalling system, many elements of which remain unknown. The sphingomyelin pathway, initiated by hydrolysis of the phospholipid sphingomyelin in the cell membrane to generate the second messenger ceramide, is thought to mediate apoptosis in response to tumour-necrosis factor (TNF)-alpha, to Fas ligand and to X-rays. It is not known whether it plays a role in the stimulation of other forms of stress-induced apoptosis. Given that environmental stresses also stimulate a stress-activated protein kinase (SAPK/JNK), the sphingomyelin and SAPK/JNK signalling systems may be coordinated in induction of apoptosis. Here we report that ceramide initiates apoptosis through the SAPK cascade and provide evidence for a signalling mechanism that integrates cytokine- and stress-activated apoptosis.

Animals↗

Construction of an insecticidal baculovirus expressing insect-specific neurotoxin AaIT.

Considering the factors which affect gene transcription, translation and the stability of mRNA, without changing the amino acid composition of the encoded polypeptide, AaIT gene encoding insect-specific neurotoxin was designed and synthesized according to bias in codon choice, overall G+C content and G+C content of bases at the third position in codons of polyhedrin genes of baculovirus and of plant genes as well. AaIT gene was fused behind a synthetic gp67 signal sequence and then recombined into the genome of Trichoplusia ni nuclear polyhedrosis virus (TnNPV) by transfer vector pSXIV VI+X3. The recombinant virus TnNPV-AaIT (occ+-gal-) was screened. The results of Southern blotting and SDS-PAGE demonstrated that AaIT gene had integrated into the genome of virus and expressed. Bioassays on the 3rd-instar Trichoplusia ni larvae showed that recombinant viruses TnNPV-AaIT could shorten the time of killing insect and improve the efficacy of killing agronomically important insects.

Animals↗

Insect-resistant tobacco plants expressing insect-specific neurotoxin AaIT.

The recombinant plant expression vector pNGY-2 with designed and synthesized AaIT gene had been constructed. The AaIT gene was fused behind the sequence of TMV and inserted into expression vector under the control of two linked 35s promoters. The recombinant plasmid pNGY-2 was transferred into tobacco NC89 by agrobacterium-mediated transfer system. The GUS activity analysis and Southern blotting of regenerated plants indicated that AaIT gene had been integrated into tobacco genome. Insect bioassays showed that some transgenic plants had notable insect-resistant activity.

Animals↗

[Pulmonary sequestration--report of 21 cases].

OBJECTIVES: To evaluate the clinical manifestation and diagnostic characteristics of pulmonary sequestration. METHOD: By retrospective analysis. RESULTS: 21 cases of pulmonary sequestration, identified by surgicea-pathologically, were reported. Only 4 cases were correctly diagnosed before operation, the other 17 cases were misdiagnosed as cyst, benign tumor or bronchiectasis. 177 cases (including the cases of our own) consist: 146 cases of intralobular type and 31 cases of extra lobular type. In 21 cases of our series, the lesions were found predominantly in the left lower lobe (13), right lower lobe (5), right upper lobe (2), right middle lobe (1). The manifestation of chest X-ray were well defined mass-like density, or cystic shadow with fluid level. CONCLUSIONS: Imaging with ultrasound, CT scan and MRI has important value in establishing a definite diagnosis by showing the anomalous artery. However, retrograde aortography plays a decisive role for confirming the diagnosis.

Adolescent↗

Effects of M1 and M2 receptor agonists and blockers on dog respiration.

AIM: To study the effects of M1 and M2 receptor agonists and blockers on dog respiration. METHODS: Using thoracic respiratory transducer and RM-86 multipurpose polygraph to determine respiratory rate (RR), tidal volume (TV), and minute ventilation volume (MVV), and DH-100G blood gas analysis instrument to analyze pO2, pCO2 and pH. RESULTS: Pilocarpine (Pil, an M1-R subtype agonist) 0.5, 1, and 2 mg.kg-1 iv caused increases in RR, MVV, and pO2, and a decrease in pCO2. The excitatory effects of Pil were antagonized by pretreatment with pirenzepine (Pir, 3 mg.kg-1, iv) and scopolamine (Sco, 2 mg.kg-1, iv). The iv injections of a novel M2-R subtype agonist, 6 beta-acetoxy nortropane (6 beta-AN) 2, 5, and 20 micrograms.kg-1 caused decreases in RR, MVV, and pO2 and an increase of pCO2. The actions of 6 beta-AN were antagonized by iv pretreatment with AF-DX116 ¿11-2 [[2-[(diethylamino)methyl]-1-piperidinyl] acetyl]-5, 11-dihydro-6H[2,3-b][1,4]benzodiazepine-6-one, 0.5 mg.kg-1¿ and atropine (Atr, 2 mg.kg-1). Similar results were obtained when smaller doses of Pil (0.2, 0.4, and 0.8 mg.kg-1) and 6 beta-AN (0.25, 0.5, and 1 microgram.kg-1) were injected into the vertebral artery. Pir and Sco also antagonized the excitatory effects of Pil, and AF-DX116 and Atr antagonized the inhibitory effects of 6 beta-AN on respiration. CONCLUSION: Stimulating M1-R of the respiratory center caused excitation of the respiration while stimulating the M2-R subtype caused inhibition of the respiration.

Animals↗

Phosphorylation of Raf by ceramide-activated protein kinase.

The sphingomyelin pathway, initiated by hydrolysis of sphingomyelin to ceramide and stimulation of a Ser/Thr ceramide-activated protein (CAP) kinase, mediates tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta action. CAP kinase is membrane-bound and proline-directed, recognizing the minimal substrate motif Thr-Leu-Pro. TNF may use the sphingomyelin pathway to signal Raf1 to activate the MAP kinase cascade. Evidence shows that cytoplasmic Raf1 binds to GTP-ras upon cellular stimulation, is recruited to the plasma membrane, and activated. How membrane-bound Raf1 is activated is uncertain, but regulation of its kinase activity may involve its phosphorylation. Specific Raf kinases, however, have not hitherto been identified. Here we report that CAP kinase phosphorylates Raf1 on Thr 269, increasing its activity towards MEK (MAP kinase or ERK kinase). Moreover, in intact HL-60 cells, CAP kinase complexes with Raf1 and, in response to TNF and ceramide analogues, phosphorylates and activates Raf1, implicating CAP kinase as a link between the TNF receptor and Raf1.

Amino Acid Sequence↗

Histamine inhibits prostaglandin E2-stimulated rabbit duodenal bicarbonate secretion via H2 receptors and enteric nerves.

BACKGROUND/AIMS: The gastroduodenal epithelium is protected from acid peptic damage by an adherent mucus-bicarbonate layer. Bicarbonate is secreted by the surface epithelial cells into this mucus layer. Patients with duodenal ulcer disease have impaired proximal duodenal bicarbonate secretion. Mast cells, present in large numbers in the duodenal mucosa, release a number of inflammatory mediators, including histamine. Release of such mast cell mediators has been implicated in ulcer disease. In this study, the ability of histamine to regulate bicarbonate secretion was examined. METHODS: Bicarbonate secretion by rabbit proximal duodenal mucosa was examined in vitro, and the effects of histamine, its agonists, and its antagonists were studied. RESULTS: Histamine essentially eliminated prostaglandin E2-stimulated duodenal mucosal bicarbonate secretion, an effect reversed both by the neurotoxin, tetrodotoxin, and the histamine H2-receptor antagonist, cimetidine, as well as reproduced by the H2-receptor agonist, dimaprit. CONCLUSIONS: In addition to the stimulatory action of histamine on gastric acid secretion, histamine expresses an additional antidefensive action by inhibiting prostaglandin E2-stimulated duodenal epithelial bicarbonate secretion. This effect of histamine is likely mediated via H2 receptors located on enteric nerves.

Animals↗

[Inhibitory effect and mechanism of scopolamine on respiration].

In conscious rabbits, dogs and anaesthetized dogs, the respiratory frequency (FR), tidal volume (Vt) and minute ventilation (Vm) were determined in order to confirm whether the respiratory effect of scopolamine is stimulatory or inhibitory. Arterial blood samples were taken intermittently and analyzed for Po2, Pco2 and pH. When scopolamine was injected i.c.v., i.a. and i.v., the decrease of FR, Vt, Vm and Po2 and the increase of Pco2 were observed in two animals. When the drug was given in clinical doses used for treating respiratory failure, the effect was seen still observable. The results indicate that scopolamine inhibits respiration. Moreover, it was observed that excitatory effect of pilocarpine on respiration can be antagonized by scopolamine, but the inhibitory effect of 6 beta-acetoxy nortropane can not be antagonized, on the contrary, can be coordinated. The above results suggest that respiratory inhibition induced by scopolamine may be related to blocking M1-R of the respiratory center.

Animals↗

Relationship between muscarinic receptor subtypes and cyclic nucleotides in pons-medulla oblongata.

AIM: To study the relationship between muscarinic receptor (M-R) subtypes and cyclic nucleotides in pons-medulla oblongata (MeOb). METHODS: The contents of cGMP and cAMP in Sprague-Dawley rat pons-MeOb, cerebellum and cerebral cortex were assayed by radioimmunoassay and competitive protein-binding assay, respectively, after ip injections of drugs. Control rats were given ip normal saline. RESULTS: M1-R agonist pilocarpine (6, 15 mg kg-1, ip) increased the content of cGMP in the pons-MeOb and cerebral cortex, but did not bring about any noticeable change in the cAMP content. The increase of cGMP was antagonized by ip pirenzepine or scopolamine. On the other hand, ip M2-R agonist 6 beta-acetoxy nortropane (6 beta-AN) 25 micrograms kg-1 reduced not only cAMP contents in the pons-MeOb and cerebellum but also cGMP contents in the pons-MeOb and cerebral cortex, while 6 beta-AN 12 micrograms kg-1 only lowered cAMP content. The decreases of cGMP and cAMP induced by 6 beta-AN were antagonized by ip AF-DX 116 or atropine, respectively. CONCLUSION: Stimulation of M1-R causes the increase of cGMP and that of M2-R induces the decreases of both cGMP and cAMP in the pons-MeOb.

Animals↗

Shared control of maltose induction and catabolite repression of the MAL structural genes in Saccharomyces.

Maltose utilization in yeast requires the presence of any one of the five unlinked, homologous MAL loci. Transcription of the two structural genes MALT (permease) and MALS (maltase) is induced by maltose and catabolite-repressed by glucose. MAL6T and MAL6S share a common 5' intergenic sequence; deletion studies within this sequence revealed a bi-directionally functioning upstream activation sequence (UASM) consisting of four 11 bp homologous sites. Activation of these sites by the MALR protein results in the coordinate expression of MAL6T and MAL6S. The basal promoter activates MALS expression to a greater extent than MALT and is located in a region that overlaps UASM. Deletion of several subsites within the UASM has an asymmetric effect on MAL gene expression, having a greater affect on MALT than on MALS. Catabolite repression of MAL6T and MAL6S by glucose is controlled at several levels. Using disruption mutants, the positively acting MAL1R protein was also found to play a role in catabolite repression of MAL6T and MAL6S.

Bacterial Proteins↗

A prospective review of 303 cementless universal cups with emphasis on wear as the cause of failure.

Three hundred thirteen primary uncemented total hip arthroplasties were performed in a 20-month period using Universal cups and Taperloc stems with titanium heads. The follow-up period was 2 to 5 years and 303 cups were measured radiographically for polyethylene wear, demarcation, osteolysis, and migration. Analysis was performed clinically, radiographically, and via inspection at revision. Twenty-three cups (7.5%) had greater than 0.5 mm polyethylene wear. Eleven of these loosened radiographically (4%) and eight (3%) required revision. All cup failures showed evidence of polyethylene wear as a contributory cause of failure. The average rate of wear was 0.5 mm/yr. Thin polyethylene liners (less than 6 mm) and titanium heads were used in all failed implants both of which have been abandoned.

Adult↗

[Inhibitory effect of 6 beta-acetoxy nortropane on respiration].

6 beta-AN (6 beta-acetoxy nortropane), a novel selective M2-receptor agonist, caused decrease in FR, TV, MVV and pO2 and increase of pCO2 when intravenous injection of 10 micrograms.kg-1 in conscious rabbits or 2, 5, 20 micrograms.kg-1 in conscious dogs was given (P < 0.05 or 0.01). The inhibitory effect on MVV exhibited a dose-dependent relationship. Small doses of 6 beta-AN icv (0.5, 1, 2, 4 micrograms.kg-1 in the conscious rabbits) and iva (0.25, 0.5 and 1.0 micrograms.kg-1 in anesthetized dogs) decreased FR, TV, MVV and pO2 and increased pCO2 as well. These results were reversed after administration of AF-DX116 and enhanced after administration of pirenzepine. Thus, it appears that the inhibitory action of 6 beta-AN on respiration might be related to stimulation of the inhibitory M2 cholinergic receptor in respiratory center.

Animals↗

The patellar "clunk" syndrome after posterior stabilized total knee arthroplasty.

In 20 patients with patellar "clunks" after posterior stabilized total knee arthroplasty, the average time to presentation was 10.7 months postarthroplasty. All patients demonstrated an audible and often painful "clunk" during extension. Fourteen procedures (11 arthroscopic debridements and three patellar component revisions) were performed in 12 patients. At reoperation, a suprapatellar fibrous nodule was seen to wedge into the intercondylar notch during flexion and dislodge during extension, generating the symptoms. The disorder resolved after nodule excision. Although four recurrences arose after arthroscopic debridements, none developed after arthrotomy and patellar button revision. Femoral component design, postsurgical inflammation, and altered extensor mechanics are potential etiologic agents of this complication.

Aged↗

Construction of glucose-repressible yeast expression vectors.

A set of two episomal yeast expression vectors, pYME1 and pYME2, were constructed. These Saccharomyces cerevisiae-Escherichia coli shuttle vectors each contain a modified yeast MAL6S (encoding maltase) promoter that is expressed constitutively, but is subject to carbon catabolite repression by glucose. Expression from this promoter is still dependent upon the presence of active MALR (regulatory) protein. These expression vectors are particularly useful because most S. cerevisiae strains are MAL+, thereby exhibiting a wider host range than GAL-based vector systems. These pYME1 and pYME2 vectors are capable of expression to levels comparable to GAL-based expression plasmids and much higher than a variety of other repressible promoter vectors. The vectors are identical, except that their multiple cloning sites (MCS) are in opposite orientations, making them convenient for inserting heterologous genes.

Base Sequence↗

The enteric nervous system modulates mammalian duodenal mucosal bicarbonate secretion.

BACKGROUND: Interaction of the enteric nerves in regulating mammalian duodenal mucosal bicarbonate secretion is not well understood. The purpose of the present experiments was to evaluate the role of the enteric nervous system on bicarbonate secretion from rabbit duodenal mucosa in vitro. METHODS: Proximal duodenum from male New Zealand White rabbits was stripped of seromuscular layers, mounted in Ussing chambers, and studied under short-circuited conditions. Effects of electrical field stimulation, vasoactive intestinal polypeptide (VIP), carbachol, prostaglandin E2 (PGE2), dibutyryl-cyclic adenosine monophosphate (db-cAMP), and the neurotoxin tetrodotoxin (TTX) and muscarinic blockade by atropine were studied. RESULTS: Electrical field stimulation significantly (P < 0.01) stimulated bicarbonate secretion, short-circuit current (Isc), and electrical potential difference (PD) that was sensitive to both TTX and atropine. VIP-stimulated bicarbonate secretion was significantly inhibited by TTX (-73%), yet Isc and PD remained unchanged. Atropine decreased VIP-induced bicarbonate secretion (-69%) and Isc (-43%). Carbachol-stimulated bicarbonate secretion, Isc, and PD were abolished by atropine, whereas TTX was without affect. Neither TTX nor atropine had a significant effect on PGE2 or db-cAMP-stimulated bicarbonate secretion. CONCLUSIONS: These results suggest that (1) enteric nerve stimulation activates an acetylcholine receptor that in turn stimulates duodenal epithelial bicarbonate secretion; (2) VIP stimulates bicarbonate secretion, in large part, via the enteric nervous system; and (3) PGE2 and cAMP stimulate bicarbonate secretion independent of the enteric nervous system.

Animals↗