Biomedical subjects

J Liu

Publications and source records attributed to J Liu.

At least 289 records · Page 16Linked to original sources

PubMed2001

Mediator proteins orchestrate enzyme-ssDNA assembly during T4 recombination-dependent DNA replication and repair.

Studies of recombination-dependent replication (RDR) in the T4 system have revealed the critical roles played by mediator proteins in the timely and productive loading of specific enzymes onto single-stranded DNA (ssDNA) during phage RDR processes. The T4 recombination mediator protein, uvsY, is necessary for the proper assembly of the T4 presynaptic filament (uvsX recombinase cooperatively bound to ssDNA), leading to the recombination-primed initiation of leading strand DNA synthesis. In the lagging strand synthesis component of RDR, replication mediator protein gp59 is required for the assembly of gp41, the DNA helicase component of the T4 primosome, onto lagging strand ssDNA. Together, uvsY and gp59 mediate the productive coupling of homologous recombination events to the initiation of T4 RDR. UvsY promotes presynaptic filament formation on 3' ssDNA-tailed chromosomes, the physiological primers for T4 RDR, and recent results suggest that uvsY also may serve as a coupling factor between presynapsis and the nucleolytic resection of double-stranded DNA ends. Other results indicate that uvsY stabilizes uvsX bound to the invading strand, effectively preventing primosome assembly there. Instead, gp59 directs primosome assembly to the displaced strand of the D loop/replication fork. This partitioning mechanism enforced by the T4 recombination/replication mediator proteins guards against antirecombination activity of the helicase component and ensures that recombination intermediates formed by uvsX/uvsY will efficiently be converted into semiconservative DNA replication forks. Although the major mode of T4 RDR is semiconservative, we present biochemical evidence that a conservative "bubble migration" mode of RDR could play a role in lesion bypass by the T4 replication machinery.

Bacteriophage T4↗

PubMed2001

Tbx19, a tissue-selective regulator of POMC gene expression.

Pituitary cell types arise in a temporally and spatially specific fashion, in response to combinatorial actions of transcription factors induced by transient signaling gradients. The critical transcriptional determinants of the two pituitary cell types that express the pro-opiomelanocortin (POMC) gene, the anterior lobe corticotropes, producing adrenocorticotropin, and the intermediate lobe melanotropes, producing melanocyte-stimulating hormone (MSH alpha), have remained unknown. Here, we report that a member of the T-box gene family, Tbx19, which is expressed only in the rostral ventral diencephalon and pituitary gland, commencing on e11.5, marks pituitary cells that will subsequently express the POMC gene and is capable of altering progression of ventral cell types and inducing adrenocorticotropin in rostral tip cells. It is suggested that Tbx19, depending on the presence of synergizing transcription factors, can activate POMC gene expression and repress the alpha glycoprotein subunit and thyroid-stimulating hormone beta promoters.

Amino Acid Sequence↗

PubMed2001

A genomewide screen for autism susceptibility loci.

We report the analysis of 335 microsatellite markers genotyped in 110 multiplex families with autism. All families include at least two "affected" siblings, at least one of whom has autism; the remaining affected sibs carry diagnoses of either Asperger syndrome or pervasive developmental disorder. Affected sib-pair analysis yielded multipoint maximum LOD scores (MLS) that reach the accepted threshold for suggestive linkage on chromosomes 5, X, and 19. Nominal evidence for linkage (point-wise P<.05) was obtained on chromosomes 2, 3, 4, 8, 10, 11, 12, 15, 16, 18, and 20, and secondary loci were found on chromosomes 5 and 19. Analysis of families sharing alleles at the putative X chromosomal linked locus and one or more other putative linked loci produced an MLS of 3.56 for the DXS470-D19S174 marker combination. In an effort to increase power to detect linkage, scan statistics were used to evaluate the significance of peak LOD scores based on statistical evidence at adjacent marker loci. This analysis yielded impressive evidence for linkage to autism and autism-spectrum disorders with significant genomewide P values <.05 for markers on chromosomes 5 and 8 and with suggestive linkage evidence for a marker on chromosome 19.

Asperger Syndrome↗

PubMed2001

New method of derivatization and headspace solid-phase microextraction for gas chromatographic-mass spectrometric analysis of amphetamines in hair.

A simple method for hair analysis of methamphetamine (MAMP) and amphetamine (AMP) by gas chromatography-mass spectrometry (GC-MS) was developed using simultaneous headspace solid-phase microextraction (HS-SPME) with derivatization. After alkaline-digestion of hair, the analytes derivatized with heptafluoro-n-butyryl chloride were adsorbed on a polydimethylsiloxane-coated fiber by HS-SPME and analyzed by GC-MS. Their mass spectra were, respectively, observable at 1 ng per sample. The standard curves in the range of 0.1-100 ng were linear. The intra-day coefficients of variation at each 0.5 ng were 12.5% for AMP and 3.8% for MAMP. The applicability of this method was demonstrated in some case studies.

Amphetamines↗

PubMed2001

Crystal structure of thiamin pyrophosphokinase.

Thiamin pyrophosphate (TPP) is a coenzyme derived from vitamin B1 (thiamin). TPP synthesis in eukaryotes requires thiamin pyrophosphokinase (TPK), which catalyzes the transfer of a pyrophosphate group from ATP to thiamin. TPP is essential for central metabolic processes, including the formation of acetyl CoA from glucose and the Krebs cycle. Deficiencies in human thiamin metabolism result in beriberi and Wernicke encephalopathy. The crystal structure of mouse TPK was determined by multiwavelength anomalous diffraction at 2.4 A resolution, and the structure of TPK complexed with thiamin has been refined at 1.9 A resolution. The TPK polypeptide folds as an alpha/beta-domain and a beta-sandwich domain, which share a central ten-stranded mixed beta-sheet. TPK subunits associate as a dimer, and thiamin is bound in the dimer interface. Despite lacking apparent sequence homology with other proteins, the alpha/beta-domain resembles the Rossman fold and is similar to other kinase structures, including another pyrophosphokinase and a thiamin biosynthetic enzyme. Comparison of mouse and yeast TPK structures reveals differences that could be exploited in developing species-specific inhibitors of potential use as antimicrobial agents.

Animals↗

PubMed2001

Cytologic artifacts and pitfalls of thyroid fine-needle aspiration using ThinPrep: a comparative retrospective review.

BACKGROUND: The ThinPrep Processor has gained popularity as a collection and preparation technique for fine-needle aspiration biopsy (FNAB). Specific cytologic criteria to evaluate ThinPrep preparation (TP) may differ from those of conventional preparation (CP). The authors retrospectively reviewed the quality, cytologic features, and pitfalls of TP versus CP in thyroid FNABs and addressed the cytomorphologic criteria used to evaluate TP specimens. METHODS: Thyroid FNABs received between January 1996-July 1999 were identified from the computer files of the Department of Pathology, University of Michigan (Ann Arbor, MI). Histologic correlation and clinical follow-up were reviewed. The cytology slides were reevaluated for cellularity, cellular preservation, artifacts, background material, architectural integrity, cytoplasmic details, and nuclear details by two observers. RESULTS: Of the 209 thyroid FNABs performed during the study period, TP and CP prepared 127 and 82 cases respectively. Histologic correlation was available in 68 (33%) cases (32 TP and 36 CP). Overall sensitivity was 80% and specificity was 98%. The sensitivity of CP versus TP was 87% and 70%, respectively. Thyroid FNABs prepared by TP, as compared with CP, were characterized by the following: The TP slide 1) allowed assessment of the overall specimen cellularity but not individual passes of an FNAB, 2) contained only "hard" colloid that appeared dense, markedly fragmented, or in droplets, 3) showed crowded, tight, tissue clusters with loss of cellular preservation, especially in the larger aggregates, 4) demonstrated more cell shrinkage, 5) showed increased disruption of the cytoplasm and numerous naked nuclei, 6) occasionally gave nucleoli a more prominent appearance, and 7) was less likely to show nuclear grooves and "pseudoinclusions" in papillary carcinoma. CONCLUSIONS: This study concluded that cytologic features used to evaluate thyroid FNABs prepared by CP may need to be modified when using TP. Awareness of the above-described findings and further studies to evaluate TP are essential to avoid potential diagnostic pitfalls.

Artifacts↗

PubMed2001

Experimental study on the fluctuations of dipolar chains.

Dynamic light scattering is used to study experimentally the dynamics of dipolar chains consisting of ferrofluid particles subjected to a magnetic field (H0). The effective diffusion coefficient shows a pronounced dependence on the scattering wave vector q, reflecting two modes of motion: translational diffusion of the whole chain, and fluctuations of particles within a chain. The characteristic probed frequency of particle displacements is inversely proportional to H0, and exhibits a q(3) dependency. Based on the striking analogy to polymer chain dynamics, we attribute these behaviors to the contribution of hydrodynamic interactions (HI's) that couples particles motion within a chain. This work suggests that chain fluctuations cannot be ignored even for the very strong magnetic field applied (coupling constant<10(6)). HI's can still be important, even at an extremely low particle volume fraction of 10(-5).

Journal Article↗

PubMed2001

[Gene diagnosis for hemophilia a using A combination of 4 techniques].

OBJECTIVE: To improve the gene diagnosis,carrier detecting and prenatal diagnosis for hemophilia A families to a maximum. METHODS: Long distance PCR (LD-PCR) was used to detect FVIII gene inversion among 26 patients with severe HA and their female offspring to identify those with FVIII gene inversion and its carriers. Three gene linkage analysis based upon PCR, Bcl I PCR/RFLP, St14 VNTR/PCR analysis and two simple dinucleotides repeats polymorphism analysis were used among 19 non-inversion HA families for indirect diagnosis. RESULTS: Sixteen families with severe HA were detected by LD-PCR among the 26 hemophilia A families. Seven were confirmed as with FVIII gene inversion (43.8%). The diagnostic rates by the above mentioned three indirect diagnostic techniques among nineteen families without gene inversion were 84.2%, 68.4% and 89.5% respectively. Confirmed diagnosis was successfully made among all of the HA families by the four techniques. CONCLUSION: Gene diagnosis and carrier detecting can be confirmed among almost all of the HA families can be diagnosed by the combined use of the four direct and indirect gene diagnostic methods.

Adolescent↗

PubMed2001

Glucose feeding exacerbates parathion-induced neurotoxicity.

Excessive dietary intake of sugars could alter various biotransformation processes and the pharmacological and toxicological properties of numerous xenobiotics. In the present study, the effects of glucose supplementation were examined on the neurotoxicity of the organophosphorus (OP) pesticide parathion (PS) and its active metabolite, paraoxon (PO), a potent inhibitor of acetylcholinesterase (AChE). Rats (n = 6-12/treatment group) were given free access to tap water or 15% glucose (w/v) in tap water beginning 7 d prior to OP toxicant exposure. Food, caloric intake, and body weight were measured daily. Animals were challenged with either PS (4.5, 9, or 18 mg/kg, sc) or PO (0.3 0.5, or 0.7 mg/kg, sc) and clinical signs of neurotoxicity (i.e., autonomic dysfunction, involuntary movements) were recorded daily for the following 13 d. Glucose feeding was associated with a dramatic drop (approximately 50%) in feed intake and an increase (approximately 20% in total caloric consumption over the 7 d prior to OP exposure. Functional toxicity associated with PS exposure was increased in glucose-fed (GF) rats, but the glucose diet had no apparent effect on clinical signs of toxicity following PO treatment. Glucose feeding increased the magnitude of AChE inhibition in the frontal cortex and plasma at lower dosages (i.e., 4.5 and 9 mg/kg) 3 d following PS treatment. Time-course studies (3, 7, and 11 d after PS exposure, 18 mg/kg, sc) indicated significantly greater brain and plasma AChE inhibition in glucose-fed animals at later time points. In contrast, glucose feeding had no effect on the degree of AChE inhibition following PO exposure. Neither liver microsomal oxidative desulfuration of PS, nor liver or plasma paraoxonase, nor liver or plasma carboxylesterase activities were measurably affected by glucose feeding. Downregulation of muscarinic receptors 7 d after PS exposure (18 mg/kg, sc) was more extensive in GF rats. It is postulated that excessiveglucose consumption decreases the intake of other dietary components, in particular amino acids, limiting the de novo synthesis of AChE and consequent recovery of synaptic transmission. Due to the shorter duration of inhibition following PO exposure, sponta neous reactivation of AChE may be more important than de novo protein synthesis in recovery of function, and thus with the effects of glucose feeding on its toxicity. Individuals that derive a large proportion of their calories from sugars may be at higher risk of acute toxicity from organophosphorus pesticides such as PS.

Animals↗

PubMed2001

Fluorescent pigments of the retinal pigment epithelium and age-related macular degeneration.

The major hydrophobic fluorophore of the retinal pigment epithelium (RPE) is A2E, a pyridinium bis-retinoid derived from all-trans-retinal and phosphatidyl-ethanolamine. The accumulation of fluorophores such as A2E is implicated in the pathogenesis of age-related macular degeneration (AMD), a disease associated with the deterioration of central vision and a leading cause of blindness in the elderly. Recent chemical and biological studies have provided insight into the synthesis and biosynthesis of A2E, the spectroscopic properties of this pigment, and the role of A2E and RPE cell death.

Age Factors↗

PubMed2001

Inactivation of CMY-2 beta-lactamase by tazobactam: initial mass spectroscopic characterization.

The CMY-2 beta-lactamase, a plasmid determined class C cephalosporinase, was shown to be susceptible to inhibition by tazobactam (K(i)=40 microM). The reaction product(s) of CMY-2 beta-lactamase with the beta-lactamase inhibitor tazobactam were analyzed by electrospray ionization/mass spectrometry (ESI/MS) to characterize the prominent intermediates of the inactivation pathway. The ESI/MS determined mass of CMY-2 beta-lactamase was 39851+/-3 Da. After inactivating CMY-2 beta-lactamase with excess tazobactam, a single species, M(r)=39931+/-3.0, was detected. Comparison of the peptide maps from tryptic digestion of the native enzyme and the inactivated beta-lactamase followed by LC/MS identified two 22 amino acid peptides containing the active site Ser64 modified by a fragment of tazobactam. These two peptides were increased in mass by 70 and 88 Da, respectively. UV difference spectra following inactivation revealed the presence of a new species with a 302 nm lambda(max). Based upon the increase in molecular mass of the tazobactam inactivated CMY-2 beta-lactamase, we propose that during the inactivation of this beta-lactamase by tazobactam an imine is formed. Tautomerization forms the spectrally observed enamine. Hydrolysis generates the covalently attached malonyl semialdehyde, its hydrate, or an enol. This work provides information on the mass of a stable enzyme intermediate of a class C beta-lactamase inactivated by tazobactam and, for the first time, unequivocal evidence that a cross-linked species is not required for apparent inactivation.

Amino Acid Sequence↗

PubMed2001

Protection of salvia miltiorrhiza against aflatoxin-B1-induced hepatocarcinogenesis in Fischer 344 rats dual mechanisms involved.

Extract of Salvia Miltiorrhiza (SM) has been widely used in traditional Chinese medicine for treating liver diseases. Recent experimental evidence indicates that it has anti-tumor potential. In this study, the effect of SM on alfatoxin B1 (AFB1)-induced hepatocarcinogenesis was investigated in male Fischer 344 rats. AFB1 (40 microg/100 g body wt, by gavage) was administered once a week for 24 weeks. In SM treatment group, rats were given SM (0.25g/100g body wt, 5 days/week by gavage) for a total of 28 weeks, including 4 weeks before and 24 weeks during AFB1 exposure. Results showed that the elevation of serum alanine aminotransferase and aspartate aminotransferase activities due to AFB1 dosing was almost completely abolished by the treatment of SM, indicating that SM could prevent AFB1-induced liver cell injury. It was further observed that SM substantially reduced glutathione S-transferase placenta form (GST-P) positive foci formation and GST-P mRNA expression caused by AFB1, which clearly suggests that SM is effective in preventing AFB1-induced hepatocarcinogenesis. Furthermore, the inhibition on AFB1 hepatocarcinigenesis was associated with a corresponding decrease in AFB1-DNA adducts formation as well as AFB1-induced oxidative DNA damage (8-hydroxydeoxyguanosine) in rat liver. Our results also indicate that the protective effect of SM might be mediated through dual mechanisms: (i) the enhancement of AFB1 detoxification pathway, especially the induction of GST-Yc2 mRNA expression, and (ii) the antioxidant property of SM.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2001

Cyanide-bridged lanthanide(III)-transition metal extended arrays: interconversion of one-dimensional arrays from single-strand (type A) to double-strand (type B) structures. Complexes of a new type of single-strand array (type C).

A series of one-dimensional arrays of lanthanide-transition metal complexes has been prepared and characterized. These complexes, [(DMF)(10)Ln(2)[Ni(CN)(4)](3)](infinity), crystallize as linear single-strand arrays (structural type A) (Ln = Sm, 1a; Eu, 2a) or double-strand arrays (structural type B) (Ln = Sm, 1b; Eu, 2b) depending upon the conditions chosen, and they are interconvertible. The single-strand type A structure can be converted to the double-strand type B structure. When the 1b and 2b type B crystals are completely dissolved in DMF, their infrared spectra are identical to the infrared spectra of 1a and 2a type A crystals dissolved in DMF. These solutions produce type A crystals initially. It is believed that formation of the type A structure is kinetically favored while the type B structure is thermodynamically favored for lanthanide-nickel complexes 1 and 2. On the other hand the complex [(DMF)(10)Y(2)[Pd(CN)(4)](3)](infinity), 3, appears to crystallize only as the double-strand array (type B). The complexes [(DMF)(12)Ce(2)[Ni(CN)(4)](3)](infinity), 4, and [(DMF)(12)Ce(2)[Pd(CN)(4)](3)](infinity), 5, crystallize as a new type of single-strand array (structural type C). This structural type is a zigzag chain array. Crystal data for 1a: triclinic space group P1, a = 10.442(5) A, b = 10.923(2) A, c = 15.168(3) A, alpha = 74.02(2) degrees, beta = 83.81(3) degrees, gamma = 82.91(4) degrees, Z = 2. Crystal data for 1b: triclinic space group P1, a = 9.129(2) A, b = 11.286(6) A, c = 16.276(7) A, alpha = 81.40(4) degrees, beta = 77.41(3) degrees, gamma = 83.02(3) degrees, Z = 2. Crystal data for 2a: triclinic space group P1, a = 10.467(1) A, b = 10.923(1) A, c = 15.123(1) A, alpha = 74.24(1) degrees, beta = 83.61(1) degrees, gamma = 83.13(1) degrees, Z = 2. Crystal data for 2b: triclinic space group P1, a = 9.128(1) A, b = 11.271(1) A, c = 16.227(6) A, alpha = 81.36(2) degrees, beta = 77.43(2) degrees, gamma = 82.99(1) degrees, Z = 2. Crystal data for 3: triclinic space group P1, a = 9.251(3) A, b = 11.193(4) A, c = 16.388(4) A, alpha = 81.46(2) degrees, beta = 77.18(2) degrees, gamma = 83.24(3) degrees, Z = 2. Crystal data for 4: triclinic space group P1, a = 11.279(1) A, b = 12.504(1) A, c = 13.887(1) A, alpha = 98.68(1) degrees, beta = 108.85(1) degrees, gamma = 101.75(1) degrees, Z = 2. Crystal data for 5: triclinic space group P1, a = 11.388(3) A, b = 12.614(5) A, c = 13.965(4) A, alpha = 97.67(3) degrees, beta = 109.01(2) degrees, gamma = 101.93(2) degrees, Z = 2.

Journal Article↗

PubMed2001

A new locus for hereditary gingival fibromatosis (GINGF2) maps to 5q13-q22.

Gingival fibromatosis (GINGF) is an oral disorder characterized by enlargement of the gingiva. It occurs either as the sole phenotype or combined with other symptoms. Thus far, one GINGF locus has been mapped on chromosome 2, at 2p21, and a second possible locus has been mapped to 2p13. However, the genes responsible for this disorder have not been elucidated. We identified a four-generation Chinese GINGF family in which the disease manifests within 1 year after birth. After exclusion of the two known GINGF loci in this family, we performed a genome-wide search to map the chromosome location of the responsible gene. We identified a new locus, GINGF2, on chromosome 5q13-q22 with a maximum two-point lod score of 4.31 at D5S1721 (theta = 0.00). Haplotype analysis placed the critical region in the interval defined by D5S1491 and D5S1453. Within this region, calcium/calmodulin-dependent protein kinase IV (CAMK4) is a strong candidate.

Age of Onset↗

PubMed2001

[Study on the improved effect of anti-TCR alpha beta monoclonal antibody on the induction of transplantation tolerance to the allogeneic skin graft in mice and its mechanisms].

OBJECTIVE: To study skin allograft tolerance induced by intravenous injection of allogeneic spleen cells and intraperitoneal injection of cyclophosphamide (CP), followed by anti-TCR monoclonal antibody injections in adult recipient mice and its mechanisms. METHODS: Injecting the spleen cells of BALB/c mice (H-2(d)) were injected to C57BL/6 mice (H-2(b), B6) via the tail vein. Two days later an intraperioneal injection of cyclophosphamide was given to the B6 mice, and followed by anti-TCR alpha beta monoclonal antibody injection via the tail vein, after which skin of BALB/c mice were grafted to the tolerance-induced B6 mice. The control groups were: (1) normal B6 mice grafted with BABL/c skin; (2) normal B6 mice grafted with KM skin; (3) B6 mice treated with SC + CP + anti-TCR alpha beta monoclonal antibody administration and grafted with BALB/c skin allograft; (4) B6 mice treated as group 3, and grafted with KM skin instead of BALB/c skin. Detection of chimerism, adoptive transfer assay and the effect of exogenous IL-2 on MLR were performed to explore tolerance mechanisms. Group data in each experiment were compared with Group's t-test. RESULTS: The survival of BALB/c skin allograft in recipient B6 mice was 66.3 days, P < 0.001 compared with the other three groups. The results of FACS analysis showed that a mixed microchimerism was developed in the thymus and spleen of tolerant mice. The percentage of cells of BALB/c origin in the thymus on day 15, 35, and 70 after induction of tolerance was 2.67%, 1.61%, and 0.47%, and in the spleen is 7.66%, 5.99%, and 3.87%, respectively. No suppressive activity in the spleen cells of tolerant mice was observed by in vivo and in vitro cell transfer experiments. MLR of spleen cells in the tolerant B6 mice to spleen cells of BALB/c origin was specifically suppressed, which was 4 725 +/- 406 cpm by (3)H-TdR incorporation. However, the specific inhibition of MLR of tolerant B6 mice could be partially reversed (P < 0.01), the (3)H-TdR incorporation reached 18 175 +/- 3 642 cpm by adding exogenous IL-2. CONCLUSION: Chimerism and clonal anergy are the main mechanisms of the tolerance.

Animals↗

PubMed2001

Phosphorylation and microtubule association of the Opitz syndrome protein mid-1 is regulated by protein phosphatase 2A via binding to the regulatory subunit alpha 4.

Opitz syndrome (OS) is a human genetic disease characterized by deformities such as cleft palate that are attributable to defects in embryonic development at the midline. Gene mapping has identified OS mutations within a protein called Mid1. Wild-type Mid1 predominantly colocalizes with microtubules, in contrast to mutant versions of Mid1 that appear clustered in the cytosol. Using yeast two-hybrid screening, we found that the alpha4-subunit of protein phosphatases 2A/4/6 binds Mid1. Epitope-tagged alpha4 coimmunoprecipitated endogenous or coexpressed Mid1 from COS7 cells, and this required only the conserved C-terminal region of alpha4. Localization of Mid1 and alpha4 was influenced by one another in transiently transfected cells. Mid1 could recruit alpha4 onto microtubules, and high levels of alpha4 could displace Mid1 into the cytosol. Metabolic (32)P labeling of cells showed that Mid1 is a phosphoprotein, and coexpression of full-length alpha4 decreased Mid1 phosphorylation, indicative of a functional interaction. Association of green fluorescent protein-Mid1 with microtubules in living cells was perturbed by inhibitors of MAP kinase activation. The conclusion is that Mid1 association with microtubules, which seems important for normal midline development, is regulated by dynamic phosphorylation involving MAP kinase and protein phosphatase that is targeted specifically to Mid1 by alpha4. Human birth defects may result from environmental or genetic disruption of this regulatory cycle.

Animals↗

PubMed2001

Hybrid nanogels for sustainable positive thermosensitive drug release.

A hybrid nanogel has been developed based on interpenetrating networks of thermosensitive poly(N-isopropylacrylamide) gels and tailored nanoporous silica. A sustainable positive thermo-responsive drug release profile is obtained. When the temperature rises, the polymer gel shrinks, squeezing the drug into the porous channels, and at the same time, opening the pores to the outside media. The drug slowly diffuses out of the porous channels. The overall release rate can be adjusted by changing the composition of the nanogel.

Acrylic Resins↗

PubMed2001

Apoptosis: one of the mechanisms that maintains unresponsiveness of the intestinal mucosal immune system.

Intestinal mucosa is constantly exposed to environmental AGS: Activation of lamina propria (LP) T cells by luminal Ags may lead to the production of inflammatory cytokines and subsequent mucosal inflammation and tissue damage. However, in normal circumstances, LP T cells do not respond to antigenic stimulation. The mechanisms of this unresponsiveness in healthy subjects are not fully understood. In this study, we found by in vivo analysis that, except for T cells in lymph nodules of the mucosa, 15% of LP T cells underwent apoptosis in normal individuals. In contrast, there was a marked reduction in apoptosis of LP T cells in patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis) and those with specific colitis. Our findings suggest that apoptosis might be a mechanism that turns off mucosal T cell responses to environmental Ags in healthy subjects, and resistance to apoptosis could be an important cause of mucosal immune dysregulation and tissue inflammation in colitis.

Apoptosis↗