Biomedical subjects

J Yu

Publications and source records attributed to J Yu.

At least 127 records · Page 7Linked to original sources

PubMed2001

[Effect of two extracted fraction from Lycopus lucidus on coagulation function].

OBJECTIVE: To find and define the effective fraction of Lycopus lucidus on coagulation. METHODS: Method of comparing turbidity, method of cutting a part of the mice tail and method of breaking glass tube. RESULTS: The two extracted fraction from lycopus lucidus F04-0A and F04-B could inhibit rats platlet aggregation in vitro and mice platelet aggregation in vivo. They could also prolong mice blood coagulation time. However, they had no effect on bleeding time. CONCLUSION: Both F04-A and F04-B had effects on inhibiting platelet aggregation and blood coagulation. Moreover, the activity of F04-A was probably stronger than that of F04-B. F04-A may be the effective fraction from Lycopus lucidus on promoting blood circulation and removing blood stasis.

Animals↗

PubMed2001

[Membranous nephropathy after allogeneic peripheral blood hematopoietic stem cell transplantation--clinicopathologic manifestations of a rare chronic GVHD].

OBJECTIVE: To investigate the clinicopathologic characteristics of renal chronic graft versus host disease (GVHD) after allogeneic peripheral blood hematopoietic transplantation(HSCT). METHODS: Clinical and pathological data from a patient with post-BMT GVHD were analysed with a related references review. RESULTS: The patient developed nephrotic syndrome (NS) 8 months after allogeneic HSCT. Renal biopsy revealed irregular thickening of glomerular basement membrane with granular deposits of IgG along it. Electronic microscopy showed electron dense deposits with increased mesangial matrix and cells in subepithelial and mesangial area. CONCLUSION: NS occurred after HSCT might be an autoimmune glomerulonephritis. Immune suppressor could reduce the incidence of NS in the HSCT patients. Cell-cept had a good efficacy in the treatment and renal biopsy played an important role in the diagnosis and prognosis of renal cGVHD.

Chronic Disease↗

PubMed2001

Alanosine (UCSD).

Researchers at the University of California at San Diego (UCSD) are developing alanosine as a potential treatment for cancer [227466], [408222]. The compound was originally under development in collaboration with Triangle, which initiated its development in 1996 [227466], but later discontinued development of the compound [406677]. As of May 2001, UCSD's ongoing clinical trials of alanosine included phase II trials for non-small cell lung cancer (NSCLC) and phase I trials for acute lymphoid leukemia (ALL), while a phase II trial for glioma at UCSD had been suspended [408222]. Alanosine is an amino acid analog originally derived from Streptomyces alanosinicus. It interferes with the de novo synthesis of adenosine in both malignant and normal cells. In cancer cells that lack methyladenosine phosphorylase (MTAP, required in the salvage pathway), alanosine should deprive such cells (but not normal cells) of de novo synthesized adenosine [277968]. In early 1997, patients were being recruited for a phase II pilot efficacy trial of alanosine as a treatment for glioma and NSCLC, since a significant number of these tumor types lack MTAP and, it was hoped, would therefore be sensitive to alanosine [239280], [248260]. Phase I and II trials were completed in the 1980s by the NCI before they were discontinued because alanosine caused toxicity typically associated with chemotherapy, and did not produce significant response rates in common tumors such as breast or colon cancers. Researchers at UCSD found that some types of cancer lack MTAP, which was responsible for alanosine's previous clinical failure [227466]; phase II trials were being carried out at the university in 1997 [269338]. Triangle obtained an option for a worldwide license from the Regents of the University of California that expired in September 1998 (but had an option to extend the period for a further one year) [277968].

Alanine↗

PubMed2001

Transcutaneous immunization: an emerging route of immunization and potent immunostimulation strategy.

Transcutaneous immunization (TCI) has emerged recently as a new method of vaccination that uses the skin. The simplicity of a patch-based immunization may obscure the potency of this strategy for immunostimulation because TCI allows the safe use of a wide variety of potent adjuvants. It is thought that these adjuvants activate Langerhans cells in the skin, which migrate to the draining lymph to orchestrate robust systemic immune responses. TCI represents a novel combination using established knowledge relating to skin penetration, the potency of adjuvant-based immunostimulation, and data showing that Langerhans cells are highly desirable targets because of their antigen-presenting cell function. The near-term challenge will be to take this promising insight into successful product development.

Adjuvants, Immunologic↗

PubMed2001

[Treatment of cerebral dural arteriovenous fistula targetting drainage vein or sinus].

OBJECTIVE: To investigate the efficacy of occluding the drainage veins or sinus in patients with cerebral dural arteriovenous fistulae. METHODS: Twenty patients with cerebral dural arteriovenous fistulae involving cavernous sinus (8), transverse-sigmoid sinus (6), tentorial sinus (3), superior sagittal (1), Galen (1) and straight sinus (1), were treated by transvenous embolization (14 patients), surgical interruption of venous drainage (5) and sinus isolation (1) respectively. RESULTS: Clinical cure was obtained in 13 patients, symptoms were relieved in 6 and aggravated in one. Angiographically, complete cure was noted in 11 patients, partial disappearance of fistulas in 9. Sixteen patients were followed up for 1-48 months. CONCLUSION: Targetting drainage vein or sinus occlusion is effective and safe in the management of patients with cerebral dural arteriovenous fistulae.

Adult↗

PubMed2001

Pathologic features of occult lymphatic metastasis in supraglottic carcinoma.

OBJECTIVE: To study the pathologic features of occult lymphatic metastasis in supraglottic carcinoma. METHODS: Serial sections of 153 neck dissection specimens in 100 patients with supraglottic carcinoma were evaluated under the microscope. RESULTS: In 100 patients, 38 had occult metastatic lymph nodes. 51 metastatic lymph nodes were found in pathology, and their sizes ranged from 0.5 cm to 2.6 cm (average 1.1 cm). The distribution of 51 lymph nodes was 1 in level I (2%), 37 in level II (73%), 12 in level III (24%), and 1 in level IV (2%). Among the 51 nodes, 21 (41%) were early stage, 18 (35%) were growth stage, 7 (14%) were tull stage, and 5 (10%) were extracapsular stage. The differentiation degree and appearance of supraglottic carcinoma was not directly related with occult metastasis. CONCLUSION: The occult metastatic rate of supraglottic carcinoma is high, and selective neck dissection may be necessary.

Adult↗

PubMed2001

[Differences of nitric oxide synthase expression and activity between splanchnic arterial and venous vessels of cirrhotic rats].

OBJECTIVE: To understand the implication of differences of nitric oxide synthase (NOS) expression and activity between splanchnic arterial and venous vessels in the pathogenesis of portal hypertension. METHODS: Cirrhosis was induced in 100 Wistar rats by subcutaneously administration of carbon tetrachloride. NOS localization, activity and gene expression in the mesenteric artery and the portal vein vessels of both cirrhotic and normal rats were investigated by immunohistochemistry, chemoluminescence and reverse transcription-polymerase chain reaction, respectively. RESULTS: There was inducible NOS enzyme isoform in al1 layers of splanchnic vessels of cirrhotic rats, whereas endothelial NOS isoform largely in vascular endothelia. NOS activity and its mRNA expression all were significantly increased in cirrhotic rats when compared with normal rats (P<0.05 or 0.01).Moreover, the activities of general and constitutive NOS and the expression of endothelial NOS mRNA in cirrhotic rats were significantly higher in the mesenteric artery than in the portal vein (P<0.01). CONCLUSIONS: Enhanced expression and activity of endothelial NOS enzyme isoform may be mainly responsible for increased NO production of splanchnic vessels in cirrhotic rats, and the differences of NOS expression and activity between the mesenteric artery and the portal vein vessels may be one of the pathogeneses of portal hypertension in which NO might be involved.

Animals↗

PubMed2001

[Research on transparent apinoid enemator].

Transparent apinoid enemator is made of polymethacrylate material. It is composed of external shell, big cover, small cover, liquor drain tube and suspension belt. Lateral surface of the shell has 100-1500 ml volume mark. Liquor drain tube is made of PVC, its inner diameter is 6 mm. The cover can reduce contamination and maintain liquor temperature. The transparent enemator made by us can overcome the shortcomings of non-transparent enamel enemator which has been used for many years.

Animals↗

PubMed2001

[Molecular tagging and mapping of QTLs for super quality fiber properties in upland cotton].

A G. anomalum introgression line, 7235, characterized as super quality fiber properties, was used to identify molecular markers linked to fiber property QTLs. By use of (7235 x TM-1)F2 in Nanjing and College Station, USA, and (7235 x TM-1)F3 in Nanjing and Hainan. Bulked segregation analysis was employed to produce 3 pairs of mixed DNA pools for fiber strength, micronaire and fiber length according to individual value of (7235 x TM-1)F2 and F2:3. A total of 221 pairs of SSR primers, 1,840 arbitrary 10-mer oligonucleotide primers and 77 ISSR primers were used to screen polymorphism between two parents, and 3 pairs of bulked DNA pools. Fifteen markers amplified by thirteen primers were identified to be linked with fiber quality QTLs through DNA polymorphism surveying between the parents, and then paired bulked DNAs, and screening the individual plant of (7235 x TM1)F2. Linkage test indicated 15 markers could be mapped to three linkage groups. In the first linkage group, eight markers (two SSR and six RAPD markers) associated with fiber strength were tightly linked with 2.2 cM interval genetic distance on average, and located on chromosome 10 in cotton. Two major QTLs for fiber quality characters were identified. One for fiber strength could explain 35% of the phenotypic variation in F2, and 53.8% in F2:3 at Hainan, which has the greatest single QTL effect of fiber strength and could be identified in all four environments, and tightly linked to 6 RAPD markers and 2 SSR markers with genetic distance no more than 16 cM in chromosome 10, in which FSRl933 is the nearest with the distance no more than 0.6 cM. One QTL linked to FMR1(603) for Micronaire could explain 7.8% of the phenotypic variation in F2, and 25.4% in F2:3 at Hainan, and expressed in all four environments. One QTL linked to FLR1(1550) for fiber length could explain 9.5% of the phenotypic variation in F2:3 at Hainan, very little in other environments. So they can be used in marker-assisted selection in increasing fiber quality of commercial cultivars.

Chromosome Mapping↗

PubMed2001

[Vasonatrin peptide attenuates hypoxia-induced increase in [Ca(2+)] (i) of culured rat cardiac fibroblasts].

The purpose of this work was to test the hypothesis that vasonatrin peptide (VNP) can attenuate the growth-promoting effect by hypoxia in cardiac fibroblasts of cultured neonatal rats. Cultured fibroblasts were divided into four groups: control group, hypoxia group, VNP group and VNP+hypoxia group. The growth of cardiac fibroblasts was observed using MTT method and the incorporation of (3)H-TdR, and the effect of VNP on the intracellular level of Ca(2+) was measured by means of interactive laser cytometry. It was found that hypoxia (2% - 3%) increased significantly the MTT optical density (OD) of cardiac fibroblasts (P<0.05 vs control group), but the increase was greatly attenuated in the VNP (10(- 6)mol/L) group and also the incorporation of (3)H-TdR in cardiac fibroblasts (P<0.05 vs hypoxia group). VNP (10(- 6)mol/L) also decreased the intracellular level of Ca(2+) which was increased by hypoxia (P<0.05) as compared with control and hypoxia group. These findings demonstrate that VNP can attenuate the hypoxia-induced growth-promoting effect in cardiac fibroblasts, which may be associated with the elevation of intracellular Ca(2+).

Animals↗

PubMed2000

Evaluation of combined fibroblast growth factor-2 and moderate hypothermia therapy in traumatically brain injured rats.

Both the exogenous administration of fibroblast growth factor-2 (FGF-2) or the induction of moderate hypothermia have been shown to attenuate histopathology and improve functional outcome after traumatic brain injury (TBI). Since combined therapeutic strategies may be more beneficial than single therapies, we examined the potential synergistic effect of FGF-2 combined with moderate hypothermia treatment induced 10 min after TBI on functional and histological outcome following controlled cortical impact (CCI) injury. Fifty male Sprague-Dawley rats were randomized to one sham and four CCI treatment groups: Sham+vehicle (VEH); FGF-2 (45 microg/kg/h for 3 h i.v.)+Normothermia (37+/-0.5 degrees C); FGF-2+Hypothermia (32+/-0.5 degrees C for 3 h); VEH+Norm; VEH+Hypo. Vestibulomotor performance on the beam balance and beam-walk (BW) tasks on post-operative days 1-5 and spatial memory acquisition in the Morris water maze (MWM) on days 14-18 were assessed. After 4 weeks survival, histological evaluations (CA(1) and CA(3) cell counts and lesion volume) were performed. MWM performance improved in all treatment groups, but combined treatment was not more efficacious than either alone. The FGF-2+Hypo group performed significantly better than the other injured treatment groups in the BW task. Lastly, no significant group differences in beam balance or histological outcome were observed. These data suggest a suboptimal and incomplete synergy of combined FGF-2 and hypothermia treatment. These data may indicate that either our dose of FGF-2 or combination therapy was not optimized in our model.

Animals↗

PubMed2000

Leisure-time physical activity, television watching, and plasma biomarkers of obesity and cardiovascular disease risk.

The benefits of physical activity in reducing cardiovascular disease (CVD) are thought to be mediated through changes in blood lipids, insulin sensitivity, and thrombogenic factors. Few studies have addressed the effects of both long-term physical activity and inactivity on these factors. The authors assessed associations between long-term leisure-time physical activity, television watching, and biomarkers of CVD risk among 468 healthy male health professionals. Prior to blood collection in 1993-1994, physical activity and television watching were assessed biennially from 1986 to 1994 by a questionnaire. Physical activity was expressed as metabolic equivalents-hours per week. Multivariate linear regression analyses showed that metabolic equivalents-hours in 1994 were significantly associated with high density lipoprotein cholesterol (HDL cholesterol) (positively) and with leptin and C-peptide (inversely). The average number of hours of television watching assessed in 1994 was significantly positively associated with low density lipoprotein cholesterol and significantly inversely associated with HDL cholesterol and apolipoprotein A1. Average hours of television watching per week assessed in 1988-1994 was positively associated with leptin levels (p < 0.01). The associations of television watching and vigorous activity with leptin and HDL cholesterol were independent of each other. In conclusion, physical activity and television watching were significantly associated with several biochemical markers of obesity and CVD risk.

Adult↗

PubMed2000

Regulation of hepatocyte thyroxine 5'-deiodinase by T3 and nuclear receptor coactivators as a model of the sick euthyroid syndrome.

The syndrome of nonthyroidal illness, also known as the sick euthyroid syndrome, is characterized by a low plasma T3 and an "inappropriately normal" plasma thyrotropin in the absence of intrinsic disease of the hypothalamic-pituitary-thyroid axis. The syndrome is due in part to decreased activity of type I iodothyronine 5'-deiodinase (5' D-I), the hepatic enzyme that converts thyroxine to T3 and that is induced at the transcriptional level by T3. The hypothesis tested is that cytokines decrease T3 induction of 5' D-I, resulting in decreased T3 production and hence a further decrease in 5' D-I. The proposed mechanism is competition for limiting amounts of nuclear receptor coactivators between the 5' D-I promoter and the promoters of cytokine-induced genes. Using primary cultures of rat hepatocytes, we demonstrate that interleukins 1 and 6 inhibit the T3 induction of 5' D-I RNA and enzyme activity. This effect is at the level of transcription and can be partially overcome by exogenous steroid receptor coactivator-1 (SRC-1). The physical mass of endogenous SRC-1 is not affected by cytokine exposure, and exogenous SRC-1 does not affect 5' D-I in the absence of cytokines. The data support the hypothesis that cytokine-induced competition for limiting amounts of coactivators decreases hepatic 5' D-I expression, contributing to the etiology of the sick euthyroid syndrome.

Animals↗

PubMed2000

In vitro sensitivity of T-cell lymphoblastic leukemia to UCN-01 (7-hydroxystaurosporine) is dependent on p16 protein status: a Pediatric Oncology Group study.

p16 regulates the cell cycle pathway by inhibiting the cyclin Ds-cyclin-dependent kinase (CDK) 4/6-mediated phosphorylation of retinoblastoma protein (pRb). Previously, we reported that most primary T-cell acute lymphoblastic leukemia (T-ALL) harbored p16 inactivation and hyperphosphorylated pRb without cyclin Ds or CDK4/6 alterations. Therefore, inhibiting CDK4/6 may be an ideal therapeutic approach for p16 (-) T-ALL. UCN-01 (7-hydroxystaurosporine) is a potent antitumor agent that exerts its effects through the inhibition of CDKs. We now report that p16 protein expression status of T-ALL cells influences their sensitivity to UCN-01. In 36 primary T-ALL cells, the IC50s of UCN-01 in the 27 p16 (-) cells (43+/-52 nM) was significantly lower than that in the 9 p16 (+) cells (258+/-260 nM). Our results suggest that agents like UCN-01 may be useful as a p16-selective therapy for T-ALL.

Alkaloids↗

PubMed2000

Role of BAX in the apoptotic response to anticancer agents.

To assess the role of BAX in drug-induced apoptosis in human colorectal cancer cells, we generated cells that lack functional BAX genes. Such cells were partially resistant to the apoptotic effects of the chemotherapeutic agent 5-fluorouracil, but apoptosis was not abolished. In contrast, the absence of BAX completely abolished the apoptotic response to the chemopreventive agent sulindac and other nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs inhibited the expression of the antiapoptotic protein Bcl-XL, resulting in an altered ratio of BAX to Bcl-XL and subsequent mitochondria-mediated cell death. These results establish an unambiguous role for BAX in apoptotic processes in human epithelial cancers and may have implications for cancer chemoprevention strategies.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2000

Do subplate neurons comprise a transient population of cells in developing neocortex of rats?

Studies were undertaken to determine whether neurons of the subplate layer represent a transient or stable population of cells in developing neocortex of rat. The first set of studies sought to determine the fraction of subplate neurons that is lost during early postnatal development. The optical dissector method was used to analyze fluorescently stained material in animals the age of postnatal day 0 (P0) to P40. These results demonstrate a reduction of slightly less than half of the total number of subplate neurons from P0 to P40. Counts of labeled cells in littermates at varied ages after [(3)H]thymidine or BRDU treatment on gestational day 14 (G14 - birthdate of occipital subplate neurons) or G18 (birthdate of layers III-IV neurons) demonstrate loss of approximately 50% of neurons in the subplate layer between P0 and P40, somewhat greater than the loss of neurons from cortical layers III-IV. The second set of studies investigated whether subplate neurons display cellular atrophy during postnatal development. Analysis of subplate neurons injected intracellularly with Lucifer yellow in fixed slice preparations indicates no reduction in soma size, number of dendrites, or extent of dendritic fields of subplate neurons taken from animals age P0 to P60. The third set of studies investigated whether functional markers of subplate neurons are reduced during postnatal development. Analysis of tissue stained histochemically for cytochrome oxidase or acetylcholinesterase, or stained immunocytochemically for GABA, somatostatin, or neuropeptide Y, demonstrate a remarkable loss of expression of staining patterns from late gestational ages to P20. These data demonstrate that, although subplate neurons seem not to be a transient population of cells in the usual sense of being eliminated by cell death or structural atrophy, the loss of histochemical and immunocytochemical markers indicates that they may be a functionally transient population of cells.

Acetylcholinesterase↗

PubMed2000

Design, synthesis, and X-ray crystal structure of a potent dual inhibitor of thymidylate synthase and dihydrofolate reductase as an antitumor agent.

A novel N-¿2-amino-4-methyl[(pyrrolo[2, 3-d]pyrimidin-5-yl)ethyl]benzoyl¿-L-glutamic acid (3a) was designed and synthesized as a potent dual inhibitor of thymidylate synthase (TS) and dihydrofolate reductase (DHFR) and as an antitumor agent. Compound 3b, the N7-benzylated analogue of 3a, was also synthesized as an antitumor agent. The synthesis of 3a was accomplished via a 12-step sequence which involved the synthesis of 2-amino-4-methylpyrrolo[2,3-d]pyrimidine (10) in 5 steps from 2-acetylbutyrolactone. Protection of the 2-amino group of 10 and regioselective iodination at the 5-position followed by palladium-catalyzed coupling afforded intermediate 14 which was converted to 3a by reduction and saponification. Similar synthetic methodology was used for 3b. X-ray crystal structure of the ternary complex of 3a, DHFR, and NADPH showed that the pyrrolo[2, 3-d]pyrimidine ring binds in a "2,4-diamino mode" in which the pyrrole nitrogen mimics the 4-amino moiety of 2,4-diaminopyrimidines. This is the first example of a classical pyrrolo[2,3-d]pyrimidine antifolate shown to have this alternate mode of binding to DHFR. Compounds 3a and 3b were more inhibitory than LY231514 against TS from Lactobacillus casei and Escherichia coli. Analogue 3a was also more inhibitory against DHFR from human, Toxoplasma gondii, and Pneumocystis carinii. Evaluation of 3a against methotrexate (MTX)-resistant cell lines with defined mechanisms indicated that cross-resistance of 3a was much lower than that of MTX. Metabolite protection studies and folylpoly-gamma-glutamate synthetase studies suggest that the antitumor activity of 3a against the growth of tumor cells in culture is a result of dual inhibition of TS and DHFR. Compound 3a inhibited the growth of CCRF-CEM and FaDu cells in culture at ED(50) values of 12.5 and 7.0 nM, respectively, and was more active against FaDu cells than MTX. In contrast, compound 3b was inactive against both cell lines. Compound 3a was evaluated in the National Cancer Institute in vitro preclinical antitumor screening program and afforded IG(50) values in the nanomolar range against a number of tumor cell lines.

Animals↗

PubMed2000

A method for determination of pyridine nucleotides using a single extract.

Intracellular redox levels play an important role in physiology and pathophysiology. The principal intracellular reductant is NADPH, which is required for both the proper activity of the entire antioxidant system and important prooxidant enzymes such as nitric oxide synthase and NADPH oxidase. Thus an easy and accurate measurement of NADPH is very desirable. The method described in this paper is based on the fact that NADH and NADPH (not NAD(+) and NADP(+)) affect absorbance at 340 nm. A single cell extract is separated into three aliquots (A(1), A(2), and A(3)). A(1) is untreated and the absorbance at 340 nm is measured. A(2) is treated with an enzyme that converts all of the NADP(+) to NADPH and then the absorbance at 340 nm is measured. A(3) is treated with an enzyme that converts all of the NADPH to NADP(+) and then the absorbance at 340 nm is measured. A(1) - A(3) is the NADPH content and A(2) - A(1) is the NADP(+) content of the extract. Using this method, we have obtained full recovery of all added nucleotides from cell extracts, thus making the method suitable for the quick determination of NADP(+) and NADPH in living cells. We conclude that this method for the measurement of NADP(+) and NADPH is rapid, simple, accurate, and reliable.

Animals↗