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Biomedical subjects

J Tan

Publications and source records attributed to J Tan.

At least 217 records · Page 12Linked to original sources
PubMed1995

Carbohydrate-deficient glycoprotein syndrome type II. An autosomal recessive N-acetylglucosaminyltransferase II deficiency different from typical hereditary erythroblastic multinuclearity, with a positive acidified-serum lysis test (HEMPAS).

Carbohydrate-deficient glycoprotein syndromes (CDGS) are a family of multisystemic congenital diseases resulting in underglycosylated glycoproteins, suggesting defective N-glycan assembly. Fibroblast extracts from two patients with a recently described variant of this disease (CDGS type II) have previously been shown to have over 98% reduced activity of UDP-GlcNAc:alpha-6-D-mannoside beta-1,2-N-acetylglucosaminyltransferase II [GlcNAc-TII; Jaeken, J., Schachter, H., Carchon, H., De Cock, P., Coddeville, B. & Spik, G. (1994) Arch. Dis. Childhood 71, 123-127]. We show in this paper that mononuclear cell extracts from one of these CDGS type-II patients have no detectable GlcNAc-TII activity and that similar extracts from 12 blood relatives of the patient, including his father, mother and brother, have GlcNAc-TII levels 32-67% that of normal levels (average 50.1% +/- 10.7% SD), consistent with an autosomal recessive disease. The poly(N-acetyllactosamine) content of erythrocyte membrane glycoproteins bands 3 and 4.5 of this CDGS patient were estimated, by tomato lectin blotting, to be reduced by 50% relative to samples obtained from blood relatives and normal controls. Similar to patients with hereditary erythroblastic multinuclearity with a positive acidified-serum lysis test (HEMPAS), erythrocyte membrane glycoproteins in the CDGS patient have increased reactivities with concanavalin A, demonstrating the presence of hybrid or oligomannose carbohydrate structures. However, bands 3 and 4.5 in HEMPAS erythrocytes have almost complete lack of poly(N-acetyllactosamine). Furthermore, CDGS type-II patients have a totally different clinical presentation and their erythrocytes do not show the serology typical of HEMPAS, suggesting that the genetic lesions responsible for these two diseases are possibly different.

Adolescent↗
PubMed1995

Anatomical compartments in the white matter of the rabbit flocculus.

The white matter of the rabbit flocculus is subdivided into five compartments by narrow sheets of densely staining acetylcholinesterase-positive fibers. The most lateral compartment is continuous with the C2 compartment of the paraflocculus and contains the posterior interposed nucleus. The other four compartments are numbered from lateral to medial as floccular compartments 1, 2, 3, and 4 (FC1-4). FC1-3 continue across the posterolateral fissure into the adjacent folium (folium p) of the ventral paraflocculus. FC4 is present only in the rostral flocculus. In the caudal flocculus FC1 and FC3 abut dorsal to FC2. Fibers of FC1-4 can be traced into the lateral cerebellar nucleus and the floccular peduncle. The presence of acetylcholinesterase in the deep stratum of the molecular layer of the flocculus and ventral paraflocculus distinguishes them from the dorsal paraflocculus. The topographical relations to the flocculus and the floccular peduncle with group y and the cerebellar nuclei are discussed.

Acetylcholinesterase↗
PubMed1995

Zonal organization of the climbing fiber projection to the flocculus and nodulus of the rabbit: a combined axonal tracing and acetylcholinesterase histochemical study.

The localization and termination of olivocerebellar fibers in the flocculus and nodulus of the rabbit were studied with anterograde axonal transport methods [wheatgerm agglutinin-horseradish peroxidase (WGA-HRP) and tritiated leucine] and correlated with the compartments in the white matter of these lobules delineated with acetylcholinesterase histochemistry (Tan et al. J. Comp. Neurol., 1995, this issue). Olivocerebellar fibers originating from the caudal dorsal cap travel through floccular compartments FC2 and FC4 to terminate as climbing fibers in floccular zones FZII and FZIV. Fibers from the rostral dorsal cap and the ventrolateral outgrowth traverse compartments FC1 and FC3, which are interleaved with compartments FC2 and FC4, and terminate in zones FZI and FZIII. Fibers from the rostral pole of the medial accessory olive traverse the C2 compartment and terminate in the C2 zone. FZI-III extend into the adjoining folium (folium p) of the ventral paraflocculus. The C2 zone continues across folium p into other folia of the ventral paraflocculus and into the dorsal paraflocculus. Four compartments and five zones were distinguished in the nodulus. Medial compartment XC1 contains olivocerebellar fibers from the caudal dorsal cap and subnucleus beta that terminate in the XZI zone. Olivocerebellar fibers from the rostral dorsal cap and the ventrolateral outgrowth occupy XC2 and terminate in XZII. The XC4 compartment contains fibers from both the caudal dorsal cap and from the rostral dorsal cap and the ventrolateral outgrowth. The latter terminate in a central portion of the XZIV zone. The dorsomedial cell column projects to the XZIII zone, which is present only in the dorsal part of the nodulus. The rostral medial accessory olive projects to the XZV zone, which occupies the lateral border of the nodulus. These results confirm and extend the conclusions of Katayama and Nisimaru ([1988] Neurosci. Res. 5:424-438) on the zonal pattern in the olivo-nodular projection in the rabbit. Additional observations were made on the presence of a lateral A zone (Buisseret-Delmas [1988] Neurosci. Res. 5:475-493) in the hemisphere of lobules VI and VII. Retrograde labeling of the nucleo-olivary tract of Legendre and Courville ([1987] Neuroscience 21:877-891) was observed after WGA-HRP injections into the inferior olive including the rostral dorsal cap and the ventrolateral outgrowth. The anatomical and functional implications of these observations are discussed.

Acetylcholinesterase↗
PubMed1995

Zonal organization of the flocculovestibular nucleus projection in the rabbit: a combined axonal tracing and acetylcholinesterase histochemical study.

With the use of retrograde transport of horseradish peroxidase we confirmed the observation of Yamamoto and Shimoyama ([1977] Neurosci Lett. 5:279-283) that Purkinje cells of the rabbit flocculus projecting to the medial vestibular nucleus are located in two discrete zones, FZII and FZIV, that alternate with two other Purkinje cell zones, FZI and FZIII, projecting to the superior vestibular nucleus. The retrogradely labeled axons of these Purkinje cells collect in four bundles that occupy the corresponding floccular white matter compartments, FC1-4, that can be delineated with acetylcholinesterase histochemistry (Tan et al. [1995a] J. Comp. Neurol., this issue). Anterograde tracing from small injections of wheat germ agglutin-horseradish peroxidase in single Purkinje cell zones of the flocculus showed that Purkinje cell axons of FZII travel in FC2 to terminate in the medial vestibular nucleus. Purkinje cell axons from FZI and FZIII occupy the FC1 and FC3 compartments, respectively, and terminate in the superior vestibular nucleus. Purkinje cell axons from all three compartments pass through the floccular peduncle and dorsal group y. In addition, some fibers from FZI and FZII, but not from FZIII, arch through the cerebellar nuclei to join the floccular peduncle more medially. No anterograde tracing experiments were available to determine the projections of the FZIV and C2 zones. The functional implications of these results are discussed.

Acetylcholinesterase↗
PubMed1995

Regulation of human T lymphocyte chemotaxis in vitro by T cell-derived cytokines IL-2, IFN-gamma, IL-4, IL-10, and IL-13.

There has been a number of conflicting reports regarding the T lymphocyte chemotactic activities of several cytokines. IL-2 and IFN-gamma are known to promote augmentation of immune inflammation, whereas IL-4, IL-10, and IL-13 display immunomodulatory effects on inflammatory cells including inhibition of cytokine production. Their effects on chemotaxis of inflammatory cells are unknown. We observed that IL-1 alpha could induce chemotaxis both in overnight cultured and anti-CD3 mAb-activated T lymphocytes and that overnight culture and anti-CD3 activation increase the number of IL-1R on T lymphocytes. In contrast, IL-8 selectively attracts freshly isolated T lymphocytes. Staurosporine inhibits freshly isolated T lymphocyte chemotaxis toward IL-8, whereas tyrphostin 23 inhibits chemotaxis of overnight cultured and anti-CD3-activated T lymphocytes toward IL-1 alpha. We have found that IL-2 and IL-13 inhibit the chemotactic migration of both CD4+ and CD8+ T lymphocytes toward IL-8, and RANTES. IL-4 inhibits only CD8+ T lymphocyte chemotaxis toward RANTES, IL-8 and IL-10. IL-10 inhibits only CD4+ T lymphocytes in their chemotactic response toward RANTES and IL-8. IFN-gamma does on the other hand augment the sensitivity of human T lymphocytes to chemotactic stimuli. Thus, our results demonstrate that different proinflammatory cytokines will induce chemotactic migration of T lymphocytes under different circumstances acting through different signaling pathways. The T cell-derived cytokines IL-2, IL-4, IL-10, and IL-13 are able to block further T lymphocyte chemotaxis, thus leading to a focusing of T lymphocytes in an area of T lymphocyte activation. These mechanisms seem relevant in our understanding of the specific and continuous localization of T lymphocytes in allergic and autoimmune disorders.

Chemokine CCL5↗
PubMed1995

T lymphocyte chemotaxis and skin diseases.

Recent advances in our understanding of the mechanisms of T lymphocyte motility and chemotaxis, particularly in aspects of lymphocyte-endothelial adhesion, transendothelial cell migration, and T-lymphocyte response to chemotactic gradients have contributed to our knowledge of how T lymphocytes accumulate during the initiation, the development and the control of inflammatory skin responses. In this review, we will summarize the present situation of studies on T lymphocyte adhesion and chemotaxis. The 3 major steps in T lymphocyte chemotaxis, e.g., recognition of extracellular chemotactic gradients, transduction into appropriate intracellular signals, and generation of motion, will be outlined. Skin-homing T lymphocytes, chemokines and other chemoattractants will also be discussed in relation to skin diseases.

Animals↗
PubMed1995

Restriction fragment length polymorphism of the T cell receptor beta-chain gene in Chinese patients with thyrotoxic hypokaleamic periodic paralysis and Graves' disease.

Restriction fragment length polymorphism (RFLP) of the T cell receptor beta-chain gene was studied in two groups of Chinese thyrotoxic patients, those with thyrotoxic hypokaleamic periodic paralysis (THPP) and those with Graves' Disease (GD). DNA digested with restriction enzymes Bgl II, Bam HI, Eco RI, Pvu II and Taq I were hybridized to a 770 bp TcR beta cDNA probe containing the joining (J) and constant (C) region segments. The TcR beta/Bgl II polymorphism of 9.2 kb and 10 kb fragments were observed in THPP, GD and normal controls. The genotype frequencies of this polymorphism, however, did not differ between patients (THPP or GD) and controls. These results, therefore, do not support the presence of an association between the TCR beta/Bgl II RFLP and THPP nor with GD susceptibility. Finally, restriction analysis of DNA from our patients and normal controls using enzymes Bam HI, Eco RI, Pvu II and Taq I with the T cell receptor beta-chain gene did not show polymorphisms, and were therefore not informative.

Adolescent↗
PubMed1995

[The effective time of HX solution for rat liver preservation].

The effects of HX solution and UW solution for rat liver preservation were studied with non-circulated isolated perfused rat liver model. Sixty-six inbred Wistar rat livers were randomly preserved for 12, 18, 24, and 30h with HX solution or UW solution. The effects were assessed by measuring hepatic tissue water content, sinusoidal lining cell mortality, Krebs-Henseleit's perfusate aspartate aminotransferase, the number of livers secreting bile during isolated perfusion, and by observing the morphological changes in liver. The experimental results suggest that the effects of HX solution for rat liver preservation be similar to those of UW solution within 24h storage.

Adenosine↗
PubMed1995

[The inhibitory effect of intraperitoneal hyperthermic and hypotonic chemotherapy on ascites cancer cells in mice].

To study the effect of inhibition of intraperitoneal hyperthermic hypotonic chemotherapy on the ascites cacer cells, LACA mice were given intraperitoneal injection of H22 cancer cells (2 x 10(7) tumor cell, each mouse). At 24 hours after the cancer injection, intraperitoneal simple hyperthermic (43 C) hypotonic fluid group (I), isotonic fluid group (II), cis-Diamminodichloroplatinum (DDP) group (IV) and hyperthermic hypotonic fluid perfusion combined with DDP group (V) were processed. The results showed that cancer cells in LACA mice peritoneal cavity were seriously damaged, the ascites growing was obviously inhibited, and the survival days of LACA mice were prolonged in all groups; however, the intraperitoneal hyperthermic hypotonic fluid perfusion with DDP group (V) presented greater effect compared with the other groups. This might be a new therapeutic procedure for the prevention and treatment of cancer ascites in the patients with digestive tract malignancies.

Animals↗
PubMed1995

[Effect of natural calcium against osteopenia in ovariectomized rats].

This study was designed to test the effect of natural calcium on the bone loss induced by ovariectomy in rats. Thirty female four-month rats were divided into three groups: sham operated group (Sham), ovariectomized group (OVX) and ovariectomized with calcium supplementation group (OVX + CA). OVX + CA rats were treated with calcium at a dose of 50 mg/kg weight per day for 90 days after surgery. Blood biochemical analysis, bone pathology, bone histomorphometric measurement and bone weight were processed. OVX rats were characterized by thinning, wormerosion like loss of trabecular bones, decreased volume of cancellous bone, increases in osteoblast index and osteoclast index, decreases in wet, dry and ash weights of left femur, and decreases in contents of calcium and phosphorus of bones. Treatment of OVX + p6 rats with calcium provided complete protection against bone loss and significantly depressed bone turnover. Our results indicate that natural calcium is effective in prevention of osteopenia in ovariectomized rats. The authors believe that the main mechanism of calcium against bone loss exists in correction of minus calcium balance, and depression of high bone turnover, especially the absorption action of osteoclasts.

Alkaline Phosphatase↗
PubMed1995

[Observation on the animal model of hypoxic-ischemic encephalopathy and the change of pathology in newborn pigs].

Thirty newborn pigs within 3 days of life were randomly divided into different groups according to the time of hypoxic-ischemic encephalopathy. The results showed that the brain damage and pathologic changes were most obvious in the 60 min hypoxia-ischemic group. Brain edema was observed in every group, especially in the group where hypoxia-ischemic lasted for more than 30 min. Cerebromalacia and hemorrhage in ventricles of brain and in arachnoid were observed, and these were particularly noticed in the group where hypoxia-ischemia lasted for 60 min.

Animals↗
PubMed1995

Detection of Mycobacterium tuberculosis in sputum, pleural and bronchoalveolar lavage fluid using DNA amplification of the MPB 64 protein coding gene and IS6110 insertion element.

Two gene sequences specific for Mycobacterium tuberculosis were evaluated for the diagnosis of pulmonary tuberculous (PTB) in pleural fluid (PF), bronchoalveolar lavage fluid (BAL) and sputum (Sp). The 240 bp sequence (nts 460-700) coding for the MPB 64 protein coding gene and the 123 bp IS6110 insertion element present in multiple copies in the mycobacterial genome were amplified using the polymerase chain reaction. Fifty-nine clinical specimens were studied. The diagnosis of PTB was confirmed by positive M. tuberculosis cultures in 14 specimens, and by the presence of characteristic histological features of granuloma and Langerhan's giant cells on pleural biopsy in 3 PF specimens through cultures for M. tuberculosis were negative. The remaining 42 specimens were obtained from patient's with non-tuberculosis pulmonary infections or malignancy, and these served as negative controls. Our results showed that the IS6110 insertion element and MPB 64 gene sequence were detected in all 14 culture positive PTB cases, although detection of the latter sequence required both DNA amplification and oligonucleotide hybridization. There was however one false positive specimen with the MPB 64 detection protocol. More importantly, both the MPB 64 sequence and IS6110 insertion element protocols were unable to detect M. tuberculosis DNA in the 3 PF samples diagnosed by histological characteristics on pleural biopsy and culture negative. We conclude that DNA amplification for M. tuberculosis-specific sequences is a useful method for rapid diagnosis of PTB in culture positive specimens. However, the false negative results with TB culture negative cases of tuberculosis pleurisy, limits its usefulness for the diagnosis of tuberculous pleurisy.

Base Sequence↗
PubMed1995

Molecular analysis of Hb Q-H disease and Hb Q-Hb E in a Singaporean family.

Hb Q (alpha 74Asp-His) results from a mutation in the alpha-gene such that abnormal alpha Q-chains are synthesized. The alpha Q-chains combine with the normal Beta A-chains to form abnormal Hb alpha 2Q beta 2A (Hb Q). Hb Q-H disease is rare, and has been reported only in the Chinese. We report here a Chinese family, were the mother diagnosed with Hb Q-H disease and the father with Hb E heterozygosity and a child with Hb Q-E-thalassemia. Thalassemia screening of the mother's blood revealed a Hb level of 6.8g/dl with low MCV and MCH. Her blood film was indicative of thalassemia. Cellulose acetate electrophoresis showed Hb H and Hb Q with the absence of Hb A. Globin chain biosynthesis was carried out and alpha Q- and beta-chains were detected. Normal alpha- chains were absent. Digestion of the mother's DNA with Bam HI and Bgl II followed by hybridization with the 1.5 kb alpha-Pst probe showed a two alpha-gene deletion on one chromosome and the -alpha Q chain mutant with the -alpha 4.2 defect on the other chromosome. DNA amplification studies indicated the two-gene deletion to be of the -SEA/ defect. The patient was concluded to possess Hb Q-H disease (--SEA/-alpha 4.2Q). Cellulose acetate electrophoresis of the father's blood showed the presence of Hb A, F and E. Molecular analysis of the father's DNA confirmed an intact set of alpha-genes (alpha alpha/alpha alpha). Globin chain biosynthesis of fetal blood of their child showed gamma, beta A, beta E, alpha A and alpha Q-chains. Molecular analysis of the child's DNA showed one alpha-gene deletion, thus giving a genotype of alpha alpha/-alpha 4.2Q beta beta E.

Base Sequence↗
PubMed1995

[Image and clinical correlative studies on cervical spinal canal stenosis].

Clinical finding, X-ray and MR imagings in 47 patients who underwent operation for degenerative cervical stenosis were correalatively studied. JOA score was used for evaluation and it varied from 6 to 14 points, with an average of 10.13 points. All Torg ratios were smaller than normal value and that of C4 was the smallest. The reserve space, sagittal diameter of spinal cord decreased, especially in the diseased segments. Sagittal diameter of spinal cord showed on T2 weighted imaging and Torg ratio were in good correlation with JOA score (P < 0.01, r = 0.4815, r = 0.0993), MRI being superior to X-ray (P < 0.01). The MRI characteristic changes of degenerative cervical stenosis were subarachnoid space decrease or vanish, compression deformation of spinal cord and abnormal signal in spinal cord. MRI classification was established according to the segments involved, compression direction. compression degree and abnormal changes in spinal cord, can indicate clinical changes and guide diagnosis and operation.

Adult↗
PubMed1995

[Production and characterization of specific monoclonal antibody against Porphyromonas endodontalis].

Porphyromonas endodontalis was known to be important microorganisms in the etiology of pulp and apical infection. In this paper, we generated hybridomas secreting monoclonal antibody against Porphyromonas endodontalis ATCC 35406. The specificity of the monoclonal antibody was examined by ELISA against a battery organisms (109 Strains). The results indicated that the monoclonal antibody did not react with any non-Porphy romanas endodontalis (104 Strains). So our monoclonal antibody is specific for Porphyromanas endodontalis and can be used in clinical samples for detection of pulp and apical infections.

Animals↗
PubMed1994

Inhibition of peptidylglycine alpha-amidating monooxygenase by N-substituted homocysteine analogs.

C-terminal amidation is a posttranslational modification found in many neuropeptides. Peptidylglycine alpha-amidating monooxygenase (PAM) catalyzes the synthesis of the biologically essential C-terminal amide from a glycine-extended precursor peptide. Reported herein are the first potent inhibitors of PAM. Dipeptides containing a C-terminal homocysteine and an N-acylated hydrophobic amino acid were found to inhibit PAM with IC50s in the low nanomolar range. Inhibition potency was dependent on both the carboxylate and the thiolate functionalities of the homocysteine and on the hydrophobic groups of the second amino acid. The thiolate was postulated to produce high binding affinities through coordination with the active-site copper. The compound series also exhibited potent inhibition of PAM in rat dorsal root ganglion cells as demonstrated by a dose-dependent increase in the substance P-Gly/substance P ratio. These results indicate that the compounds have sufficient potency and intracellular bioavailability to aid future studies focused on neuropeptide function and the contributions of neuropeptides to various disease processes.

Animals↗
PubMed1994

Selective destruction of gliomas in immunocompetent rats by thymidine kinase-defective herpes simplex virus type 1.

BACKGROUND: Thymidine kinase-deficient herpes simplex virus type 1 [tk(-) HSV-1] replicates well in dividing cells but not in nondividing cells such as neurons, suggesting a potential use in the treatment of brain tumors. PURPOSE: We attempted to examine the efficacy of using tk(-) HSV-1 for treating brain tumors in immunocompetent animals. METHODS: 9L glioma cells were cultured and subsequently implanted intracerebrally in immunocompetent, adult male Long-Evans rats. A thymidine kinase-defective HSV-1 virus, KOS-SB, was used to infect 9L cells in culture, and the viability of the infected cells was compared with that of mock-infected (i.e., uninfected) cells. We also injected the virus intratumorally and determined the mortality of the tumor-bearing animals. Tumor regression and viral spread following virus injection were examined by histologic and immunocytochemical assays. RESULTS: In vitro, the tk(-) virus destroyed cultured 9L cell monolayers at multiplicities of infection of 0.1 and 1.0 within 48 hours. With the same quantity of virus, no remarkable difference in survival of neural cells was found. Foscarnet, an antiviral drug that acts independently of tk activity, blocked viral replication by greater than 99% at a concentration of 100 micrograms/mL. The mortality of animals bearing tumors declined with an increase in the amount of virus injected. Histologic examination showed that the HSV-1 treatment caused severe tumor regression. Immunocytochemistry using an anti-HSV-1 antibody revealed only a weak staining within the regressing tumors, and few immunopositive neurons were evident in the surrounding brain tissue. CONCLUSIONS: The results indicate that tk(-) HSV-1 mutants can selectively and effectively destroy glioma cells both in vitro and in vivo in normal, immunocompetent animals. IMPLICATIONS: Our failure to detect viral spread associated with regressing tumors suggests that some other cytopathic factors might be involved in the tumor regression. Regardless of the precise mode of tumor cell killing, HSV-1 may be useful for treating brain tumors.

Animals↗