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Biomedical subjects

L Fan

Publications and source records attributed to L Fan.

At least 73 records · Page 4Linked to original sources
PubMed2000

Study on polymorphism of MICA exon 5 microsatellite in Shanghai Han population.

OBJECTIVE: To investigate the polymorphism distribution of MICA gene exon 5 microsatellite in Shanghai Han population and study the relationship of MICA gene and its closely linked gene HLA B. METHODS: The microsatellite polymorphism of MICA exon 5 in 175 unrelated healthy individuals were investigated using PCR-heteroduplex analysis. RESULTS: (1)There are 5 alleles of the microsatellite polymorphism in exon 5 of the MICA gene in Shanghai Han population, the gene frequency of MICA*A5 is the highest(39.14%), the next is MICA*A5.1(22.29%). (2)There is strong linkage disequilibrium between the HLA-B and MICA STR loci, e.g. MICA*A5 and HLA-B15, MICA*A4 and HLA-B27. CONCLUSION: The polymorphism distribution of MICA gene and the linkage disequilibrium between MICA and HLA-B have deviations in different ethnic groups.

China↗
PubMed2000

[Study on normal pregnancy and recurrent spontaneous abortions from helper T cell 1/helper T cell 2 cytokines balance].

OBJECTIVE: To investigate the function of Th1 (IFN-gamma, TNF-alpha) and Th2 (IL-4, IL-10) cytokine balance in the maternal-fetal tolerance. METHODS: The IFN-gamma, TNF-alpha, IL-4 and IL-10 mRNA were studied from PBMCs of 11 normal non-pregnancy control, 10 women in first trimester of normal pregnancy, 11 women in last trimester of normal pregnancy by semi-quantitative reverse transcriptional-polymerase chain reaction (RT-PCR) method. RESULTS: (1) The IFN-gamma mRNA decreased [(24.68 +/- 5.55)%, P < 0.05], while the IL-10 mRNA rose [(20.72 +/- 5.36)%, P < 0.01] in normal pregnancy women compared with the non-pregnancy control [IFN-gamma(30.76 +/- 5.35)%, IL-10 (13.58 +/- 3.91)%]. (2) IL-10 mRNA decreased [(9.48 +/- 2.84)%, P < 0.05], while the IFN-gamma mRNA rose [(36.08 +/- 5.75)%, P < 0.05] in RSA women compared with the non-pregnancy control. (3) The IFN-gamma mRNA rose (P < 0.01), while the IL-10 mRNA decreased (P < 0.01) in RSA women compared with women in their first trimester of normal pregnancy [IFN-gamma(27.23 +/- 5.74)%, IL-10 (18.61 +/- 5.43)%]. CONCLUSIONS: The results suggest that women in normal pregnancy had mainly the Th2 cytokines. The breakage of the Th1/Th2 balance may result in RSA. The results provide clue that Th1/Th2 balance plays a role in maternal-fetal tolerance.

Abortion, Habitual↗
PubMed2000

[A study on the deficiency of anticoagulant proteins in Chinese patients with deep venous thrombosis].

OBJECTIVE: To investigate the incidence of anticoagulant proteins deficiency in Chinese patients with venous thrombosis. METHODS: Eighty-seven patients with otherwise unexplained venous thrombophilia were studied. Both the antigen and antivitity of PC, PS, and antithrombin III (ATIII) were determined using commercial kits (Stago, or IL) activated PC, sensitivity ratio (APC-SR) by Coatest chromogenix, and factor V gene mutation by polymerase chain reaction with restriction fragments long polymorphism (PCR-RFLP). RESULTS: Of all the patients twenty-five were found to be abnormal. These consisted of 3 ATIII deficiencies, 5 PC deficiencies, 10 PS deficiencies, 2 resistance of activated protein C (APC-R), 1 combined ATIII and PC deficiency, 1 combined ATIII and PS deficiency, 1 combined PC and PS deficiency, 1 combined APC-R and PC deficiency and 1 combined APC-R and PS deficiency. The overall prevalence of ATIII, PC and PS deficiencies was 26.4%. The patients with anticoagulant proteins deficiency had earlier onset (35.2 +/- 9.7 vs 42.1 +/- 10.9; P < 0.01) and more recurrent thrombosis (P < 0.05), as well as more pulmonary embolism (44.0% vs 16.1%; P < 0.01) than those of without anticoagulant protein deficiency. CONCLUSION: The overall prevalence of ATIII, PC, and PS deficiency in Chinese venous thrombosis patients was higher than that of Western patients. It suggests that the etiology of thrombophilia may be different between Chinese and Western.

Adolescent↗
PubMed2000

[Endometrial stromal sarcoma with multi-differentiation: a study of 17 cases].

OBJECTIVE: To investigate the clinical and pathomorphological features of multi-differentiated endometrial stromal sarcoma of the uterus and to discuss their behaviour and differential diagnosis. METHODS: The histological characteristics of all cases were observed by pathological examination, some of them have been studied by immunohistochemical and/or ultrastructural techniques. RESULTS: Multi-differentiation was present in 13 cases of low grade and 4 cases of high grade endometrial stromal sarcoma, of which, 13 cases had sex-cord differentiation, 10 cases had smooth muscle differentiation, osseous differentiation in 2 cases and striated muscle differentiation in 1 case. Two types of multi-differentiation was present in 9 cases. CONCLUSIONS: Both low-grade and high-grade endometrial stromal sarcoma of uterus can display multi-differentiation. Sex-cord and smooth muscle differentiation are the most common types. Osseous and striated muscle differentiation are very rare. There is no definite correlation between prognosis and the amount or types of multi-differentiation components.

Adult↗
PubMed2000

[Evaluation of hearing thresholds of 40Hz auditory event related potential and auditory brainstem response].

Recordings of pure tone response, 40 Hz auditory event-related potential (40 Hz AERP) and auditory brainstem response (ABR) were obtained for 74 ears of 42 cases (32 normal ears, 42 injured ears). 40 Hz AERP (0.5-2 kHz) of 20 ears was tested under natural sleep and awake conditions. The results showed that the threshold of 40 Hz AERP was higher than that of tone pip, with the difference of 12.7 +/- 6.4 dBnHL at 0.5 kHz, 14.7 +/- 6.3 dBnHL at 1 kHz, and 15.6 +/- 5.6 dBnHL at 2 kHz respectively. The threshold of 40 Hz AERP increased in natural sleep compared with that in awake state. The threshold of ABR was higher than the behavioral. The data suggests that jointly using several tests get more accurate and objective results in evaluating hearing loss.

Adolescent↗
PubMed1999

Construction and characterization of polycistronic retrovirus vectors for sustained and high-level co-expression of apolipoprotein A-I and lecithin-cholesterol acyltransferase.

Apolipoprotein A-I (apo A-I) and lecithin-cholesterol acyltransferase (LCAT) are constituents of circulating high-density lipoprotein (HDL) particles and play an important role in 'reverse cholesterol transport', the process by which cholesterol in peripheral tissues is transferred to the liver for excretion. Enhancing levels of apo A-I, as well as LCAT, in plasma may promote the removal of excess cholesterol from the arterial wall and thus reduce the formation of atherosclerotic lesions. Indeed, both apo A-I and LCAT genes have been identified as therapeutic targets to prevent or limit atherogenesis. Here, we have constructed two retroviral vectors, one containing LCAT cDNA and the neomycin phosphotransferase (NEO) gene (pLLEN), the other apo A-I cDNA, LCAT cDNA and the NEO gene (pLAPLEN) linked by internal ribosome entry sites (IRES). Both bi- and tricistronic retroviral vectors efficiently co-expressed their two or three genes when transfected into cultured mouse C2C12 muscle cells or human 293 cells. After 30 days, the retroviral vector sequences were retained by the host cells, whereas those of a conventional plasmid vector were lost. Moreover, transduced C2C12 mouse myoblasts maintained the ability for heterologous expression of human LCAT and apo A-I even after differentiation into myotubes. Stably-transduced clones of C2C12 cells were selected by neomycin (G418) resistance and continued to efficiently express human LCAT for 60 days. These findings indicate that the use of polycistronic retrovirus vectors to genetically modify myoblasts, which can be transplanted back into skeletal muscle, might be a safe and feasible strategy to express human apo A-I and LCAT and hence have therapeutic potential to regress atherosclerotic lesions.

Animals↗
PubMed1999

Smoking in China: findings of the 1996 National Prevalence Survey.

CONTEXT: As the world's largest producer and consumer of tobacco products, China bears a large proportion of the global burden of smoking-related disease and may be experiencing a tobacco epidemic. OBJECTIVE: To develop an evidence-based approach supporting tobacco control initiatives in China. DESIGN AND SETTING: A population-based survey consisting of a 52-item questionnaire that included information on demographics, smoking history, smoking-related knowledge and attitudes, cessation, passive smoke exposure, and health status was administered in 145 disease surveillance points in the 30 provinces of China from March through July 1996. PARTICIPANTS: A nationally representative random sample of 128766 persons aged 15 to 69 years were asked to participate; 120298 (93.8%) provided data and were included in the final analysis. About two thirds of those sampled were from rural areas and one third were from urban areas. MAIN OUTCOME MEASURES: Current smoking patterns and attitudes; changes in smoking patterns and attitudes compared with results of a previous national survey conducted in 1984. RESULTS: A total of 41187 respondents smoked at least 1 cigarette per day, accounting for 34.1% of the total number of respondents, an increase of 3.4 percentage points since 1984. Current smoking continues to be prevalent among more men (63%) than women (3.8%). Age at smoking initiation declined by about 3 years for both men and women (from 28 to 25 years). Only a minority of smokers recognized that lung cancer (36%) and heart disease (4%) can be caused by smoking. Of the nonsmokers, 53.5% were exposed to environmental tobacco smoke at least 15 minutes per day on more than 1 day per week. Respondents were generally supportive of tobacco control measures. CONCLUSION: The high rates of smoking in men found in this study signal an urgent need for smoking prevention and cessation efforts; tobacco control initiatives are needed to maintain or decrease the currently low smoking prevalence in women.

Adolescent↗
PubMed1999

Improved artificial death switches based on caspases and FADD.

A number of "suicide genes" have been developed as safety switches for gene therapy vectors or as potential inducible cytotoxic agents for hyperproliferative disorders, such as cancer or restenosis. However, most of these approaches have relied on foreign proteins, such as HSV thymidine kinase, that primarily target rapidly dividing cells. In contrast, novel artificial death switches based on chemical inducers of dimerization (CIDs) and endogenous proapoptotic molecules function efficiently in both dividing and nondividing cells. In this approach, lipid-permeable, nontoxic CIDs are used to conditionally cross-link target proteins that are fused to CID-binding domains (CBDs), thus activating signaling cascades leading to apoptosis. In previous reports, CID-regulated Fas and caspases 1, 3, 8, and 9 were described. Since the maximum efficacy of these artificial death switches requires low basal and high specific activity, we have optimized these death switches for three parameters: (1) extent of oligomerization, (2) spacing between CBDs and target proteins, and (3) intracellular localization. We describe improved conditional Fas and caspase 1, 3, 8, and 9 alleles that function at subnanomolar levels of the CID AP1903 to trigger apoptosis. Further, we demonstrate for the first time that oligomerization of the death effector domain of the Fas-associated protein, FADD, is sufficient to trigger apoptosis, suggesting that the primary function of FADD, like that of Apaf-1, is oligomerization of associated caspases. Finally, we demonstrate that nuclear-targeted caspases 1, 3, and 8 can trigger apoptosis efficiently, implying that the cleavage of nuclear targets is sufficient for apoptosis.

Adaptor Proteins, Signal Transducing↗
PubMed1999

The accessory subunit of mtDNA polymerase shares structural homology with aminoacyl-tRNA synthetases: implications for a dual role as a primer recognition factor and processivity clamp.

The accessory subunit of the heterodimeric mtDNA polymerase (polgamma) from Drosophila embryos is required to maintain the structural integrity or catalytic efficiency of the holoenzyme. cDNAs for the accessory subunit from Drosophila, man, mouse, and rat have been identified, and comparative sequence alignment reveals that the C-terminal region of about 120 aa is the most conserved. Furthermore, we demonstrate that the accessory subunit of animal polgamma has both sequence and structural similarity with class IIa aminoacyl-tRNA synthetases. Based on sequence similarity and fold recognition followed by homology modeling, we have developed a model of the three-dimensional structure of the C-terminal region of the accessory subunit of polgamma. The model reveals a rare five-stranded beta-sheet surrounded by four alpha-helices with structural homology to the anticodon-binding domain of class IIa aminoacyl-tRNA synthetases. We postulate that the accessory subunit plays a role in the recognition of RNA primers in mtDNA replication, to recruit polgamma to the template-primer junction. A similar role is served by the gamma-complex in Escherichia coli DNA polymerase III, and indeed our accessory subunit model shows structural similarity with the N-terminal domain of the delta' subunit of the gamma-complex. Structural similarity is also found with E. coli thioredoxin, the accessory subunit and processivity factor in bacteriophage T7 DNA polymerase. Thus, we propose that the accessory subunit of polgamma is involved both in primer recognition and in processive DNA strand elongation.

Amino Acid Sequence↗
PubMed1999

Hyperplasia in multiple smooth muscle tissues in transgenic mice expressing a temperature-sensitive SV40 T-antigen under the control of smooth muscle alpha-actin regulatory sequences.

Control of smooth muscle cell (SMC) proliferation is of fundamental importance in the development and pathology of the vasculature. To derive vascular SMC with conditional inactivation of negative cell cycle regulatory proteins in the context of smooth muscle protein expression, a 3.4 kb fragment of the mouse SMC alpha-actin promoter was used to target a temperature-sensitive mutant SV40 T antigen (tsA58) to smooth muscle in transgenic mice. Mice with this genotype display a heritable phenotype of abnormal SMC proliferation in the central tail artery, vasa deferentia, seminal vesicles, prostate, and uterus, with the latter resembling uterine leiomyomatosis and prostatic hypertrophy. Neither the aorta nor other viscera manifested abnormal proliferation. Cultures from aorta, vas deferens, seminal vesicle, and kidney tissue were characterized with regard to protein expression, stability, and matrix remodelling capacity. The alpha-actin content/cell was up to 3-4-fold higher, as well as more stable than in primary SMC cultures, suggesting successful selection for propagation of cells expressing this differentiation marker. All cells displayed enhanced growth at the permissive temperature. As an initial functional assessment, the cells were compared to non-transformed mouse aortic SMC with respect to the ability to remodel collagen gel matrices, and demonstrated conservation of this physiologic function. This in vivo analysis of the SMC alpha-actin promoter supports a broader range of smooth muscle-directed expression activity than previously recognized, and establishes the feasibility of its use to direct transgene expression to vascular as well as genito-urinary smooth muscle. The targeted expression of the tsA58 T antigen has yielded transgenic animals with several manifestations of smooth muscle hyperplasia; these animals have in turn permitted the derivation of several murine SMC lines with phenotypic stability and conditionally-modulated proliferation. These cells will allow expansion of derivative transfected smooth muscle cell lines under permissive conditions, as well as oncogene inactivation at the restrictive temperature when desired for functional studies.

Actins↗
PubMed1999

Mutations in Sabin 2 strain of poliovirus and stability of attenuation phenotype.

In this study, we attempted to identify the molecular determinants in the genome of the attenuated Sabin 2 vaccine strain of poliovirus that may change during vaccine production and result in an increase in monkey neurovirulence. An extensive search for suitable vaccine lots identified six batches that had failed the monkey neurovirulence test (MNVT). On repeated tests, these batches were found to have acceptable levels of monkey neurovirulence. One of the batches was additionally passaged six times under conditions used in vaccine production, and the resulting high-passage sample was screened for the presence of mutations and tested in monkeys. In addition to the previously described A --> G reversion at nucleotide 481, high-passage stock also contained a mutation in the VP1-coding region (3364 = G --> A) that consistently accumulated in the course of passaging. However, despite the presence of substantial amounts of these mutations, high-passage stock passed the MNVT. Replication of Sabin 2 poliovirus in the central nervous system of transgenic mice susceptible to poliovirus or in cultures of mouse cells, resulted in another mutation (3363 = A --> G). Even though its presence correlated with paralysis in mice, the introduction of 3363-G into the Sabin 2 genome did not increase neurovirulence of the virus. Previous studies identified the 481-G mutation as an important determinant of monkey neurovirulence. We prepared virus samples with varying amounts of genetically defined single mutants at this nucleotide and tested them in monkeys. The results demonstrated that even a 100% substitution at this site introduced into Sabin 2 strain did not increase monkey neurovirulence. The determination of the nucleotide sequence of an alternative strain used for the production of type 2 OPV (Chung 2) showed that it contained 100% of the wild-type 481-G but possessed an extremely low level of neurovirulence. These results demonstrate the remarkable stability of the attenuated phenotype of the Sabin 2 strain and show that (1) no batch of OPV 2 has ever repeatedly failed the MNVT, (2) growing the virus beyond the passage level allowed in vaccine production did not result in increased neurovirulence in monkeys, (3) a test for neurovirulence in transgenic mice may be more sensitive than the MNVT, and (4) determination of the mutational profile of vaccine batches detects inconsistencies in vaccine manufacturing processing that would not be detected by the MNVT.

5' Untranslated Regions↗
PubMed1999

Self-reactive T cells selected on thymic cortical epithelium are polyclonal and are pathogenic in vivo.

Positive selection of CD4+ T cells requires that the TCR of a developing thymocyte interact with self MHC class II molecules on thymic cortical epithelium. In contrast, clonal deletion is mediated by dendritic cells and medullary epithelium. We previously generated K14 mice expressing MHC class II only on thymic cortical epithelium. K14 CD4+ T cells were positively, but not negatively, selected and had significant in vitro autoreactivity. Here, we examine the function of these autoreactive CD4+ T cells in more detail. Analysis of a series of K14-derived T hybrids demonstrated that the autoreactive population of CD4+ T cells is phenotypically and functionally diverse. Purified K14 CD4+ T cells transferred into lethally irradiated wild-type B6 mice cause acute graft vs host disease with bone marrow failure. Further, these autoreactive CD4+ T cells cause hypergammaglobulinemia and the production of autoantibodies when transferred into unirradiated wild-type hosts. Thus, positive selection by normal thymic cortical epithelial cells, unopposed by negative selection, produces polyclonal CD4+ T cells that are pathologic.

Acute Disease↗
PubMed1999

Dual mechanisms of regulation of Na/H exchanger NHE-3 by parathyroid hormone in rat kidney.

Parathyroid hormone (PTH) is a potent inhibitor of mammalian renal proximal tubule sodium absorption via suppression of the apical membrane Na/H exchanger (NHE-3). We examined the mechanisms by which PTH inhibits NHE-3 activity by giving an acute intravenous PTH bolus to parathyroidectomized rats. Parathyroidectomy per se increased apical membrane NHE-3 activity and antigen. Acute infusion of PTH caused a time-dependent decrease in NHE-3 activity as early as 30 min. Decrease in NHE-3 activity at 30 and 60 min was accompanied by increased NHE-3 phosphorylation. In contrast to the rapid changes in NHE-3 activity and phosphorylation, decrease in apical membrane NHE-3 antigen was not detectable until 4-12 h after the PTH bolus. The decrease in apical membrane NHE-3 occurred in the absence of changes in total renal cortical NHE-3 antigen. Pretreatment of the animals with the microtubule-disrupting agent colchicine blocked the PTH-induced decrease in apical NHE-3 antigen. We propose that PTH acutely cause a decrease in NHE-3 intrinsic transport activity possibly via a phosphorylation-dependent mechanism followed by a decrease in apical membrane NHE-3 antigen via changes in protein trafficking.

Amino Acid Sequence↗
PubMed1999

Early neuronal expression of tumor necrosis factor-alpha after experimental brain injury contributes to neurological impairment.

Tumor necrosis factor-alpha (TNF alpha) is a pleiotropic cytokine involved in inflammatory cascades associated with CNS injury. To examine the role of TNF alpha in the acute pathophysiology of traumatic brain injury (TBI), we studied its expression, localization and modulation in a clinically relevant rat model of non-penetrating head trauma. TNF alpha levels increased significantly in the injured cortex at 1 and 4, but not at 12, 24 or 72 h after severe lateral fluid-percussion trauma (2.6-2.7 atm). TNF alpha was not elevated after mild injury. At 1 and 4 h after severe TBI, marked increases of TNF alpha were localized immunocytochemically to neurons of the injured cerebral cortex. A small population of astrocytes, ventricular cells and microvessels, also showed positive TNF alpha staining, but this expression was not injury-dependent. Macrophages that were present in a hemorrhagic zone along the external capsule, corpus callosum and alveus hippocampus at 4 h after TBI did not express TNF alpha. Intracerebroventricular administration of a selective TNF alpha antagonist--soluble TNF alpha receptor fusion protein (sTNFR:Fc) (37.5 microg)--at 15 min before and 1 h after TBI, improved performance in a series of standardized motor tasks after injury. In contrast, intravenous administration of sTNFR:Fc (0.2, 1 or 5 mg/kg) at 15 min after trauma did not improve motor outcome. Collectively, this evidence suggests that enhanced early neuronal expression of TNF alpha after TBI contributes to subsequent neurological dysfunction.

Animals↗
PubMed1999

Acute inhibition of Na/H exchanger NHE-3 by cAMP. Role of protein kinase a and NHE-3 phosphoserines 552 and 605.

Regulation of the renal Na/H exchanger NHE-3 by protein kinase A (PKA) is a key intermediate step in the hormonal regulation of acid-base and salt balance. We studied the role of NHE-3 phosphorylation in this process in NHE-deficient AP-1 cells transfected with NHE-3 and in OKP cells expressing native NHE-3. A dominant-negative PKA-regulatory subunit completely abolished the effect of cAMP on NHE-3 activity demonstrating a role of PKA in the functional regulation of NHE-3 by cAMP. NHE-3 isolated from cAMP-treated cells showed lower phosphorylation by purified PKA in vitro suggesting that NHE-3 is a PKA substrate in vivo. Although changes in NHE-3 whole protein phosphorylation is difficult to detect in response to cAMP addition, the tryptic phosphopeptide map of in vivo phosphorylated NHE-3 showed a complex pattern of constitutive and cAMP-induced phosphopeptides. To test the causal relationship between phosphorylation and activity, we mutated eight serines in the cytoplasmic domain to glycine or alanine. Single or multiple mutants harboring S552A or S605G showed no PKA activation or reduced regulation by PKA activation. Ser-552 and Ser-605 were phosphorylated in vivo. However, multiple mutations of serines other than Ser-552 or Ser-605 also reduced the functional PKA regulation. We conclude that regulation of NHE-3 by PKA in vivo involves complex mechanisms, which include phosphorylation of Ser-552 and Ser-605.

Amino Acid Substitution↗
PubMed1999

[Studies on the factors affecting the individual's animal protein intake by a multi-level model].

In this article, the influence of factors related to different levels (seg, provincial, county and household) on the proportion of protein intake from animal food was evaluated by using multi-level modeling. It was found that after being adjusted by individual factors, the factors related to the household, such as household income, dietary habit and knowledge of nutrition were the most important factors affecting the individual's showed animal protein intake. In addition, the results showed that the difference of animal protein intake in various places depended not only on the increase of household income, but also dietary behavior and agriculture crops in different areas. Comparison of different models indicates that in analyzing the data from large-scale health survey with hierchical structure, multi-level modeling is strongly recommended.

Adolescent↗
PubMed1999

Immunohistochemical localization of vascular endothelial growth factor in the globule leukocyte/mucosal mast cell of the rat respiratory and digestive tracts.

Vascular endothelial growth factor (VEGF) is a potent angiogenic mitogen that also increases vascular permeability. Immunohistochemical localization of VEGF in the respiratory and digestive tracts of healthy adult rats was investigated at light and electron microscopic levels using a specific antibody. The results revealed solitary cells with strong VEGF immunoreactivity scattered in the epithelium of the respiratory tract as well as in the lamina propria and epithelium of the intestine. From ultrastructural features of their large cytoplasmic granules, VEGF-positive cells in the respiratory tract were identified as globule leukocytes (GL). The immunoreactivity was localized exclusively in the cytoplasmic granules of GL. Most of the VEGF-positive cells in the small intestine were located in the lamina propria, whereas those in the large intestine were found more frequently in the epithelium than in the lamina propria. They showed the same morphological features as respiratory tract GL and were identified as mucosal mast cells (MMC). When examined in serial sections, GL/MMC in the respiratory and digestive tracts showed only weak reactivity to anti-histamine antibody. In contrast, connective tissue mast cells (CTMC), which were located in the submucosa of the digestive tract and in the connective tissues of the respiratory tract and other organs, were intensely immunopositive for histamine, whereas they showed no reactivity to anti-VEGF antibody. The specific occurrence of VEGF in GL/MMC suggests that this cell type is involved in paracrine regulation of the permeability of nearby microvessels, and that VEGF immunoreactivity can be used as a histochemical marker to distinguish GL/MMC from CTMC.

Animals↗