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Biomedical subjects

S Cai

Publications and source records attributed to S Cai.

At least 91 records · Page 5Linked to original sources

[Invasion behavior of hepatocellular carcinoma cells correlates with their rheological properties].

We investigated the viscoelasticity, mechanics of adhesion to collagen I coated surfaces and mechanics of adhesin to liver sinosoidal endothelial cells(LECs) among primary culture human hepatocytes, hepatocellular carcinoma(HCC) cells as well as HCC-Inv cells, namely HCC cells capable of invading the artificial basement membrane, Matrigel. The results showed that the above-mentioned rheological properties of HCC cells differed obviously from those of normal hepatocytes. HCC-Inv cells exhibited higher viscoelastic coefficients, higher adhesion forces to collagen I coated surfaces as well as higher adhesion forces to LECs than those of normal hepatocytes and HCC cells. Immunocytochemistry showed the differences in cell morphology and cytoskeleton structure between HCC cells and HCC-Inv cells. A brief discussion was presented in relation to the changes in cell rheological properties of hepatocellular carcinoma cells and their pathological significance.

Carcinoma, Hepatocellular↗

[Histological study of the local-regional invasion of pyriform sinus carcinoma].

OBJECTIVE: In order to offer the basis for the operation of the pyriform sinus carcinoma, the local-regional invasion patterns of the pyriform sinus carcinoma were investigated. METHODS: Twenty-six surgical specimens obtained from patients who undergone laryngopharyngectomy were subjected to a whole organ section study. RESULTS: Tumors located in the lateral wall of the pyriform sinus spread mainly towards the lateral wall of the hypopharynx. Tumors located in the inner wall of the pyriform sinus spread mainly towards the larynx and opposite side pyriform sinus, the paraglottic space and thyroid cartilage were particularly frequent invaded. It was rare of the invading of the cricoid cartilage. The invasion of the epiglottis and preepiglottic space across the midline had not been found. There were two invading routines, the paraglottic space and preepiglottic space. The invasion of the paraglottic space was through the aryepiglottic fold and the inner surface of the thyroid cartilage. The invading of the preepiglottic space was through the aryepiglottic fold and the upper part of the inner surface of the thyroid cartilage. CONCLUSIONS: The invading of the preepiglottic space was not the contraindication of the partial laryngectomy. It is practicable to preserve the laryngeal function in most of the patients while tumors located on the lateral or inner wall of the pyriform sinus. There was a tendency to the invading to the contralateral side in the inner wall of the pyriform or postcricoidarytenoid region. Attention should be paid to the submucosal spreading in the postcricoidarytenoid region.

Adult↗

[Studies on the infrared spectra of clusters containing O3MoS3, [Mo(x) (CO)y(O,S-C6H4-1,2)3FezLm]n- (x = 1,2 or 3, y = 0,3,7 or 4, z = 0 or 1, L = Cl, m = 0,2, n = 1 or 2) unit and the relationship between the spectra and their structures].

The IR spectra of clusters containing O3MoS3 Unit, (Et4N) [Mo(O, S-C6H4-1,2)3](1), (Et4N)2[Mo2(CO)3(O,S-C6H4-1,2)3](2), (Et4N)2[Mo3(CO)7(O,S-C6H4-1,2)3](3) and (Et4N)2[Mo2(CO)4(O,S-C6H4-1,2)3FeCl2](4) have been investigated. The characteristic frequencies, nu (Mo(n+)-OtR) (n = 4,5), nu (Mo(n+)-ObR) (n = 0,4), nu (Mo(n+)-StR) (n = 4,5), nu (Mo(n+)-SbR)(n = 0,1,4), nu (C = O), nu (Mo(n+)-C)(n = 0,1), delta (Mo(n+)-C-O)(n = 0,1), nu (Fe(2+)-ObR) and nu (Fe(2+)-Cl) were assigned by comparing the vibrational frequencies and structure parameters of them with that of Mo-Fe-S clusters. The influences of sigma donor abilities of ligands L(-OR, -SR) on nu (Mo-C) and nu (C = O) and the effect of Mo(n+)-->Mo4+ (n = 0,1) charge transfer on nu (Mo(4+)-ObR), nu (Mo(n+)-C) and nu (C = O) have been discussed. A partial oxidation of cluster 4 to [Mo2(CO)3(O,S-C6H4-1,2)3]- (5) have been inferred according to the information from the changes of IR spectra of cluster 4 in air with time and the existence of cluster 5 was also verified by NFAB-MS of cluster 4.

English Abstract↗

Perforin pathway is essential for protection of mice against lethal ocular HSV-1 challenge but not corneal scarring.

Perforin (cytolysin; pore-forming protein) is expressed in both CD8(+) cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, and is a major factor responsible for the cytolytic activities of these cells. Both CD8(+) T-cells and NK cells are important in eliminating cells infected with certain viruses. We examined the role of perforin in a mouse model of HSV-1 infection using perforin-deficient mice. Naïve perforin knockout (perforin(0/0)) mice were more susceptible to lethal HSV-1 ocular challenge (60% survival), than naïve parental C57BL/6 (100% survival). In contrast, both C57BL/6 and perforin(0/0) mice had similar levels of HSV-1 induced corneal scarring. Vaccination of perforin(0/0) mice induced a significantly higher HSV-1 neutralizing antibody titer than vaccination of C57BL/6 mice, and the mice were completely protected against lethal ocular challenge. These results suggest that in naïve mice ocularly challenged with HSV-1, the perforin pathway was involved in protection against death, but not in protection against corneal scarring.

Animals↗

Serotonin receptor subtypes that depolarize guinea pig inferior mesenteric ganglion neurons.

Our previous studies indicated that serotonin (5-HT) depolarized a majority of guinea pig inferior mesenteric ganglion (IMG) neurons and may be another transmitter for the noncholinergic late slow excitatory postsynaptic potential (ls-EPSP) in the IMG. However, the subtypes of 5-HT receptor mediating these responses have not yet been identified. Using intracellular recording, we examined the effect of 5-HT receptor antagonists with specificity to various 5-HT receptor subtypes on the 5-HT-mediated depolarization and ls-EPSP in IMG neurons in vitro. Cyproheptadine, a 5-HT(1/2) receptor antagonist, reversibly inhibited the slow, but not the fast, depolarization and ls-EPSP in the 5-HT-sensitive neurons. Both mianserin and spiperone, 5-HT(2) and 5-HT(1A) receptor antagonists, did not significantly alter either the fast or slow depolarizing responses or the ls-EPSP. The 5-HT(3) receptor antagonist MDL 72222 (Bemesetron) completely inhibited the fast depolarization with little diminution of the slow depolarization and ls-EPSP. Superfusion of putative 5-HT(1P) receptor antagonist, BRL 24924 (Renzapride), reversibly attenuated both the depolarization and ls-EPSP. However, 5-HT-insensitive neurons with ls-EPSP were found to be insensitive to both cyproheptadine and BRL 24924. In most 5-HT-sensitive neurons, the 5-HT(3) receptor agonist, 2-methyl-5-HT, and the selective 5-HT(1P) agonist, MCPP or 5-OHIP, evoked a fast and a slow depolarization in 55.6 and 71.4% of the neurons, respectively, without a significant effect on the membrane potential in 85.7 and 100% of the 5-HT-insensitive neurons. In 5-HT-sensitive neurons, MDL 72222 reversibly abolished the fast depolarization induced by 2-methyl-5-HT; BRL 24924 significantly inhibited the slow depolarization induced by MCPP or 5-OHIP, but not by SP. Prolonged superfusion of 5-HT-sensitive neurons with MCPP abolished the evoked ls-EPSP without inhibition of action potential. These results suggest that the fast and slow depolarizations in these neurons are mediated by 5-HT(3) and 5-HT(1P) receptor subtypes, respectively. The latter may also mediate the ls-EPSP in 5-HT-sensitive neurons.

Animals↗

Identification of beta-turn and random coil amide III infrared bands for secondary structure estimation of proteins.

Fourier transform infrared spectroscopy is increasingly becoming an important method to determine secondary structure of peptides and proteins. Among the spectral regions arising out of coupled and uncoupled stretching and bending modes of amide bonds, amide I and amide III spectral bands have been found to be the most sensitive to the variations in secondary structure folding. Amide I spectral region (1700-1600 cm-1), although most commonly used primarily because of its strong signal, suffers from several limitations, including a strong interference from water vibrational band, relatively unstructured spectral contour, and overlap of revolved bands correspondingly to various secondary structures. In contrast, amide III spectral region (1350-1200 cm-1), albeit relatively weak in signals, does not have the above limitations. Easily resolved and better defined amide III bands are quite suitable for quantitative analysis of protein secondary structure. While amide III region has been successfully used for determination of alpha-helix and beta-sheets (Fu, F.-N., et al. (1994) Appl. Spectrosc. 48, 1432-1441), bands corresponding to beta-turns and random coils have not been identified, so far. In this paper, we describe, for the first time, identification of amide III bands corresponding to beta-turns and random coils by selectively enhancing random coils by treatment with a denaturing reagent, and secondary structure estimation of several proteins by using the band assignments. The assignments of spectral bands were as follows: 1330-1295 cm-1, alpha-helix; 1295-1270 cm-1, beta-turns; 1270-1250 cm-1, random coils; and 1250-1220 cm-1, beta-sheets. The estimations of secondary structural elements by the above assignments correlated quite well with secondary structure estimations from X-ray crystallography data.

Amides↗

Specific and nonspecific immune stimulation of MHC-II-deficient mice results in chronic HSV-1 infection of the trigeminal ganglia following ocular challenge.

Ocular herpes simplex virus type 1 (HSV-1) infection of MHC-II-deficient mice (AO/Obeta mice) or their parental C57BL/6J wild-type mice resulted in the establishment of typical HSV-1 latent infections in the trigeminal ganglia (TG) of the surviving mice by day 28 postinfection. Latency was characterized by the complete absence of infectious virus in TG extracts, the ability to recover latent virus only following prolonged tissue culture cultivation of explanted TG, and the presence of HSV-1 DNA in TG extracts. When mice were vaccinated prior to ocular HSV-1 challenge, latency appeared unaltered in the C57BL/6J wild-type mice. However, in AO/Obeta mice, clearance of virus from the TG appeared to be seriously impaired, resulting in a chronic productive infection, rather than a latent infection. Infectious virus was readily detected in TG extracts of vaccinated AO/Obeta mice until at least 63 days postinfection. Glycoprotein B mRNA was also readily detected, confirming continued viral transcription. These chronic infections occurred regardless of whether the AO/Obeta mice were vaccinated with HSV-1-specific antigens (i.e., live HSV-1 strain KOS, recombinantly expressed HSV-1 glycoprotein D plus Freund's adjuvant, or a mixture of seven recombinantly expressed HSV-1 glycoproteins plus adjuvant) or non-HSV-1-specific antigens (i.e., tissue culture medium plus 5% fetal bovine serum, the expression vector plus adjuvant, or adjuvant alone). Passive transfer of HSV-1 neutralizing antibody to vaccinated AO/Obeta mice between days 0 and 28 post-ocular challenge did not clear infectious virus from the TG. Passive transfer of anti-HSV-1 antibody or purified naive mouse serum to unvaccinated AO/Obeta mice on days 3 or 6 post-HSV-1 ocular challenge also resulted in chronic, rather than latent, infection of the TG. Passive transfer of naive sera from B-cell-deficient mice or injection of keyhole limpet hemocyanin or purified IgG, but not PBS or dextran, 3 days after HSV-1 challenge also resulted in chronic infection of the TG.

Animals↗

Vaccination with different HSV-1 glycoproteins induces different patterns of ocular cytokine responses following HSV-1 challenge of vaccinated mice.

We previously reported that vaccination of BALB/c mice with different baculovirus expressed HSV-1 glycoproteins induced varying degrees of protection against HSV-1 ocular challenge, ranging from complete protection to no protection, to exacerbation of eye disease. To correlate specific local immune responses with protection and exacerbation of corneal scarring, we examined immune cell infiltrates in the cornea after ocular HSV-1 challenge of vaccinated mice. Mice were vaccinated with gD, which completely protects against corneal scarring, gG, which produces no protection against corneal scarring, or gK, which exacerbates corneal scarring. Cryostat sections of cornea were taken at different times after challenge and examined for infiltrating cells containing IL-2, IL-4, IFN-gamma, IL-6, or TNF-alpha. No corneal infiltrates were seen before challenge or 1 day after ocular challenge in any groups. By days 3-7, many cells containing IL-4 and IFN-gamma, but few cells containing IL-2, had infiltrated into the corneas of gG or mock vaccinated mice. At the same times, many cells containing IL-2, but few cells containing IL-4 or IFN-gamma, were seen in the corneas of gD vaccinated mice. In contrast, the corneas of mice vaccinated with gK contained large amounts of IL-2, IFN-gamma, and IL-4. Our results suggest that: (1) corneas from gD vaccinated mice had no corneal disease and developed a response highly biased toward IL-2 responses; (2) corneas from gG or mock vaccinated eyes had significant corneal disease and developed a mostly IL-4 and IFN-gamma cytokine response; and (3) corneas from gK vaccinated mice had exacerbated corneal disease and developed strong IL-2, IL-4 and IFN-gamma cytokine responses.

Animals↗

Enhancement of the endopeptidase activity of botulinum neurotoxin by its associated proteins and dithiothreitol.

Botulinum neurotoxins type A (BoNT/A), the most toxic substance known to man, is produced by Clostridium botulinum type A as a complex with a group of neurotoxin-associated proteins (NAPs), possibly through a polycistronic expression of a clustered group of genes. The botulinum neurotoxin complex is the only known example of a protein complex where a group of proteins (NAPs) protect another protein (BoNT) against acidity and proteases of the GI tract. We now report that NAPs also potentiate the Zn2+ endopeptidase activity of BoNT/A in both in vitro and in vivo assays against its known intracellular target protein, 25 kDa synaptosomal associated protein (SNAP-25). While BoNT/A exhibited no protease activity prior to reduction with dithiothreitol (DTT), the BoNT/A complex exhibited a high protease activity even in its nonreduced form. Our results suggest that the bacterial production of NAPs along with BoNT is designed for the NAPs to play an accessory role in the neurotoxin function, in contrast to their previously known limited role in protecting the neurotoxin in the GI tract and in the external environment. Structural features of BoNT/A change considerably upon disulfide reduction, as revealed by near-UV circular dichroism spectroscopy. BoNT/A in the reduced form adopts a more flexible structure than in the unreduced form, as also indicated by large differences in DeltaH values (155 vs 248 kJ mol-1) of temperature-induced unfolding of BoNT/A.

Animals↗

Drug interactions with diosmectite: a study using the artificial stomach-duodenum model.

Drug interactions with diosmectite, a gastric-protective drug, were studied in vitro using an artificial stomach-duodenum model. The behavior of neutral and ionisable drugs with pKa values ranging between 2 and 8 was monitored to determine the physicochemical characteristics of the interactions. The main neutral (digoxin) and acid (valproic acid) drug substances were moderately fixed by clay (<27%), in a pH-independent manner. Basic compounds with a pKa<7 (dapsone, metronidazole, cimetidine) were strongly fixed in acid medium (?62%), and fully released under neutral conditions. Amphoteric (fluoroquinolones) and basic compounds with a pKa>/=7 (ranitidine, pyrimethamine) were adsorbed by more than 81% by diosmectite in gastric and duodenal compartments. In the part of the model representing the distal duodenum, the potential site for drug absorption, only the active substances which remained positively charged (amphoteric and basic compounds) showed a large reduction (>/=80%) in their available free fraction. Ionisation of drug substances administered per os concomitantly with diosmectite plays a crucial role in these interactions.

Adsorption↗

Urinary N-acetyl-beta-D-glucosaminidase isoenzymes as biomarker of renal dysfunction caused by cadmium in a general population.

N-Acetyl-beta-D-glucosaminidase (NAG) and its isoenzymes in urine have been studied in a population group residing in a polluted area in China. The area studied was contaminated by industrial wastewater from a nearby smelter that discharged cadmium-polluted wastewater into a river used for the irrigation of rice fields. Cadmium concentrations in rice were 3.70, 0.51, and 0.07 mg/kg for the highly and moderately polluted areas and the control area, respectively. Cadmium concentrations in urine exceeded 5 microgram/liter in the majority of subjects in the most highly polluted area. There was a marked dose-dependent increase in NAG and NAG B content of urine related both to urinary cadmium and to the calculated cadmium uptake. It is concluded that urinary NAG and its isoenzymes could serve as a sensitive biomarker of renal dysfunction in cadmium-exposed populations. The mechanisms underlying the increase in NAG and its isoenzymes after cadmium exposure need to be studied further.

Acetylglucosamine↗

Intranuclear relocalization of matrix binding sites during T cell activation detected by amplified fluorescence in situ hybridization.

We describe a method for analyzing the nuclear localization of specific DNA sequences, with special emphasis on their binding status to the nuclear matrix, depending on the developmental stage of the cells. This method employs high-resolution fluorescence in situ hybridization procedures. For our studies, it was important to examine the nuclear localization of a particular gene locus. Previously, however, it was not possible to detect a single-copy genomic sequence using a DNA probe less than several kilobases in size. We describe here a signal amplification technique based on tyramide which makes such a task possible. Using this method, we monitored single-copy loci using a short, 509-bp DNA sequence that binds in vivo to the T cell factor SATB1 within T cell nuclei, high-salt-extracted nuclei (histone-depleted nuclei generating "halos" with distended chromatin loops), and the nuclear matrix, before and after T cell activation. We found that these loci were anchored onto the nuclear matrix, creating new bases of chromatin loops, only after T cell activation. This experimental strategy, therefore, enabled us to detect the changes in higher order chromatin structure upon activation and study gene regulation at a new dimension: the loop domain structure. The methods shown here can be widely applied to explore other functions involving chromatin, including recombination and replication.

Binding Sites↗

Saikosaponins from roots of Bupleurum scorzonerifolium.

Saikosaponin u and saikosaponin v, were isolated from the roots of Bupleurum scorzonerifolium and these saponins were identified as 3-O-[beta-D-glucopyranosyl-(1-->2)-beta-D-glucopyranosyl- (1-->3)-beta-D-fucopyranosyl]-3 beta,16 alpha,23,28-tetrahydroxy-olean- 11,13(18)-dien-30-oic acid-30-O-[pentito(1-->1)-beta-D-glucopyranosyl-(6-->)] ester and 3-O-[beta-D-glucopyranosyl-(1-->3)-beta-D-fucopyranosyl]-3 beta,16 alpha,23,28-tetrahydroxy-olean-11,13(18)-dien-30-oic acid-30-O-[pentito(1-->1)-beta-D-glucopyranosyl(6-->)] ester, respectively.

Anti-Inflammatory Agents, Non-Steroidal↗

The role of interleukin (IL)-2 and IL-4 in herpes simplex virus type 1 ocular replication and eye disease.

To assess the relative effect of interleukin (IL)-2- and IL-4-dependent immune responses on herpes simplex virus (HSV)-1 infection, naive, vaccinated, and mock-vaccinated IL-20/0 and IL-40/0 knockout mice were challenged ocularly with HSV-1. Naive IL-20/0 mice were significantly more susceptible to lethal infection than IL-40/0 or parental BALB/c mice. Vaccinated, IL-20/0, IL-40/0, and BALB/c mice induced similar neutralizing antibody titers and were completely protected against HSV-1-induced death and corneal scarring. Vaccinated and mock-vaccinated IL-20/0 mice had significantly higher HSV-1 titers in their eyes than BALB/c mice, while vaccinated and mock-vaccinated IL-40/0 mice had significantly lower HSV-1 titers in their eyes than BALB/c mice. Recombinant (r) IL-2 treatment of the IL-20/0 mice significantly reduced ocular HSV-1 replications, but rIL-4 treatment of IL-40/0 mice significantly increased ocular HSV-1 replications. Th1 (IL-2) cytokine responses may help protect mice against ocular HSV-1 challenge and reduce ocular HSV-1 replication.

Animals↗

Effects of oxidative damage of membrane protein thiol groups on erythrocyte membrane viscoelasticities.

In three oxidative damaging systems: the diamide-mercaptoethanol redox modification system (DM), the pyrogallol oxygen free radicals system (PG) and the hypoxanthine-xanthine oxidase oxygen free radical system (HXO), the effect of erythrocyte membrane oxidative damage on membrane viscoelasticities was investigated with micropipette aspiration method. The experimental results indicated that erythrocyte membrane oxidative damage has a great influence upon the membrane mechanical properties. The oxidative damage led to decrease of contents of membrane protein thiol radical. The scanning of SDS-PAGE presented that membrane proteins form the higher molecular weight component (HMP) by the cross-linking of membrane protein thiol radicals that might hinder the conformational change of membrane protein. This might be the reason for the increased membrane elastic modulus and viscous coefficient upon treating erythrocytes with the oxidative damaging systems. A significant negative logarithm regression relation was found between the membrane elastic modulus, mu, or viscoefficient, eta, and the contents of membrane protein thiol radicals. These experimental results suggested that thiol radicals oxidative damage reaction due to the superoxides anions (*O2-) may be an important molecular mechanism inducing changes of membrane viscoelasticities or whole cell deformability of erythrocyte under physiological and pathological oxidative stress.

Blood Viscosity↗