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Biomedical subjects

C C Tseng

Publications and source records attributed to C C Tseng.

At least 91 records · Page 5Linked to original sources
PubMed1993

Met-8 of the beta 1-bungarotoxin phospholipase A2 subunit is essential for the phospholipase A2-independent neurotoxic effect.

beta 1-Bungarotoxin consists of a phospholipase A2 subunit and a non-phospholipase A2 subunit. The toxin was oxidized with a 100-fold molar excess of chloramine T with respect to the methionine content of the protein in 0.1 M Tris/HCl at pH 8.5 and at room temperature. Reactivities of the two methionine (Met-6 and Met-8 of the phospholipase A2 subunit), five histidine, 14 tyrosine and one tryptophan residues of one toxin molecule with chloramine T were assessed from the change in intrinsic fluorescence and amino acid composition of the protein. Met-8 and one tyrosine on the phospholipase A2 subunit and less than one histidine were oxidized, while Met-6 remained intact after 30 min of reaction. One histidine and approx. two tyrosine residues were oxidized when both methionine residues were oxidized after 90 min of reaction. The sole tryptophan was oxidized slightly throughout the reaction. The chloramine T oxidation did not destroy the two Ca(2+)-binding domains, though it modified the toxin to become less effective at binding Ca2+. The modified toxin obtained after 30 or 90 min reaction time retained 65% or 40% of the phospholipase A2 activity of the parent toxin, but both were not lethal to mice and showed a very weak ability to induce the indirectly evoked contraction of chick biventer cervicis muscle. It is suggested that Met-8 may play an important role in the phospholipase A2-independent interaction with the nerve terminal membrane during the neurotoxic effect of beta 1-bungarotoxin.

Animals↗
PubMed1993

Glucose-dependent insulinotropic peptide: structure of the precursor and tissue-specific expression in rat.

Glucose-dependent insulinotropic peptide (GIP) is a 42-amino acid gastrointestinal regulatory peptide that stimulates insulin secretion from pancreatic beta cells in the presence of glucose. Approximately 7.8 x 10(5) recombinant clones of a neonatal rat intestinal cDNA library were screened by using plaque hybridization, and three clones were identified and sequenced with the dideoxynucleotide chain-termination method. The translated amino acid sequence deduced from the nucleotide sequence of the cDNA indicated that rat GIP was derived by proteolytic processing of a 144-amino acid precursor polypeptide. The mature peptide is flanked by a 43-amino acid NH2-terminal peptide that contains a 21-amino acid signal peptide and by a 59-amino acid COOH-terminal peptide. Analysis of the nucleotide and amino acid sequence of rat GIP revealed only two substitutions from the known human GIP peptide. The use of high-stringency RNA blot-hybridization analysis of total RNA extracted from various organs demonstrated expression of the GIP gene in the duodenum and jejunum and, to a lesser extent, in the ileum. In addition, expression of the GIP gene was observed in the submandibular salivary gland both by RNA analysis and RIA. In response to duodenal perfusion of a 20% Lipomul meal for 60 min, duodenal mucosal GIP mRNA concentrations increased by 42.8% and 48.2% at 30 and 60 min, respectively.

Amino Acid Sequence↗
PubMed1993

Inhibitory effects of a cholecystokinin antagonist, loxiglumide (CR-1505), on the growth of freshly separated and xenografted human pancreatic cancer.

The effects of cholecystokinin (CCK) and a CCK antagonist, loxiglumide (CR-1505), on four freshly separated and six xenografted human pancreatic cancers, were investigated. The level of DNA synthesis in only one of five tested pancreatic cancers was enhanced by CCK at concentrations of 0.01-10 nM, while in the other four cancers DNA synthesis was not affected. The levels of DNA, RNA, and protein synthesis (by 3H-thymidine, 3H-uridine, and 3H-leucine incorporation tests, respectively) in all the tested cancers were dose-dependently inhibited by loxiglumide at concentrations of 20-2000 microM, and the IC50 of loxiglumide for DNA synthesis in pancreatic cancers was 156 +/- 80 microM (means +/- SD). The in vivo effect of loxiglumide was assessed using a xenografted line (PC-HN) transplanted in nude mice. The in vivo 50% lethal dose of loxiglumide for nude mice was about 500 mg/kg. Death was caused by respiratory failure due to severe congestion of the lung after the administration of a large dose of loxiglumide. The growth of a PC-HN transplanted in the nude mice was significantly inhibited by subcutaneous loxiglumide at 250 mg/kg, twice a day for 28 days, which did not cause death. It is suggested that loxiglumide inhibits the in vivo and in vitro growth of human pancreatic cancer, perhaps independently of its action as a CCK antagonist, and this study also suggests that loxiglumide may be a new type of therapeutic agent to be used for the treatment of human pancreatic cancer.

Animals↗
PubMed1993

Acute cocaine toxicity: the effect of agents in non-seizure-induced death.

Death from cocaine intoxication results from one or more of the multiple mechanisms including seizures, cardiovascular collapse, or apnea. In the free-moving rat model, continuous seizures are a major cause of death. To study other mechanisms of death unrelated to seizures in this model, we suppressed lethal seizures with diazepam (DZP) and investigated the effect of several pharmacological agents. Rats were pretreated with vehicle alone, diazepam 5 mg/kg alone, or a combination of DZP plus either nifedipine (NIFD) 2 mg/kg, propranolol (PROP) 10 mg/kg, or prazosin (PRAZ) 5 mg/kg. Five minutes after pretreatment, all animals received cocaine 100 mg/kg. Each test group consisted of 15 animals and all agents were given IP. Two animals in each group had cortical electrodes implanted. Animals that received vehicle followed by cocaine had 100% incidence of seizures and death. Those rats that received DZP alone followed by cocaine had no seizures and 53% death. Rats that received DZP plus NIFD or DZP plus PROP had suppression of seizures but no significant change in the incidence of death. The group that received DZP and PRAZ followed by cocaine had no seizures and 13% incidence of death (p < 0.001). Electroencephalogram recordings showed cortical electrical spike activity or spike-and-wave afterdischarges in all animals clinically observed to have seizures. In the absence of clinical seizure activity, no significant cortical spike activity was noted. It is concluded that animals protected from seizures with diazepam can still have nonseizure deaths after high-dose cocaine. The incidence of death in these animals is not reduced with nifedipine or propranolol pretreatment but is reduced with prazosin pretreatment.

Animals↗
PubMed1993

A phase II study of 5-fluorouracil, cisplatin, and 4'-epirubicin in the treatment of advanced solid cancers.

This phase II study was designed to assess the therapeutic potential of intensive course treatment with three anticancer agents: 50 mg of cisplatin on day 1, 40 mg/m2 of epirubicin on day 2, and 250 mg of 5-fluorouracil on days 2 through 5. Drug courses were repeated every 2 weeks and most patients received between 4 and 6 courses. Thirty-five patients with measurable advanced solid cancers entered the study. They consisted of 16 gastric, 5 colorectal, 4 gallbladder, 3 pancreatic, 3 lung, 2 esophageal, 1 uterine, and 1 ovarian cancers. Of the 35 patients, 29 were evaluated for therapeutic effect of the regimen, and the overall response rate was 31.0% (5 CR + 4 PR/29). A 33.3% rate of tumor regression, consisting of 2 complete responses (CR) and 3 partial responses (PR) out of 15 patients (2 CR + 3 PR/15), was seen for gastric cancers. For the other types of tumors the responses were achieved in 2 lung cancers (1 CR + 1 PR/3). 1 uterine cancer (1 CR/1), and 1 ovarian cancer (1 CR/1). The esophageal, colorectal, pancreatic, and gallbladder cancers were unresponsive to this regimen. Toxicities of the drug treatment were clinically tolerable and consisted of general malaise, nausea, vomiting, stomatitis, alopecia, and leucopenia. However, two patients died of uncontrollable metabolic acidosis after 1 and 2 courses, respectively. This intensive course treatment appears to promote the regression of gastric, lung, and gynecologic cancers.

Adult↗
PubMed1993

In vitro and in vivo activities of Q-35, a new fluoroquinolone, against Mycoplasma pneumoniae.

The in vitro potency and in vivo efficacy of Q-35, a new fluoroquinolone, against Mycoplasma pneumoniae were investigated by pharmacokinetic studies with M. pneumoniae-infected hamsters. By using fluoroquinolones, macrolides, and tetracyclines as references, Q-35 was found to possess the greatest mycoplasmacidal activity. The MIC for 90% of strains tested (MIC90) and the MIC50 were 0.78 and 0.39 microgram/ml, respectively, and the MBC for 90% of strains tested (MBC90) and the MBC50 were 3.13 and 0.78 microgram/ml, respectively. The MBC50-to-MIC50 ratio for Q-35 was 2. Furthermore, only Q-35 continued to be effective against 19 strains of erythromycin-resistant mutants of M. pneumoniae. The efficacies of fluoroquinolones against M. pneumoniae were also investigated by using an experimental hamster pneumonia model to measure the CFU of M. pneumoniae in the lungs. Q-35 and ofloxacin were efficacious following oral administration of 200 mg/kg/day for 5 days, initiated 24 h after infection, while ciprofloxacin was not active. Continuous administration of Q-35 for 10 days significantly reduced numbers of viable M. pneumoniae in the lungs. These results suggest that both Q-35 and ofloxacin are effective in the early phase of infection and, moreover, that Q-35 is also effective in the middle stage of infection, when progressive lung alterations and continuous increases in mycoplasmal growth occur. Peak levels of Q-35 in sera and lungs after oral administration were higher than those of ciprofloxacin but lower than those of ofloxacin. On the basis of these results, Q-35 appears to be a promising antimicrobial agent in chemotherapy of mycoplasmal infection.

Administration, Oral↗
PubMed1993

Incidence of clinical infection after periodontal surgery: a prospective study.

The purpose of this study was to evaluate the incidence of clinical infection after routine periodontal surgery. The population studied comprised patients in need of periodontal surgery at the Periodontal Division, Dental Department, National Cheng Kung University Hospital, during the period from January 1989 to June 1990. A total of 207 patients including 103 males and 104 females were involved, and 220 surgical procedures were carried out under aseptic conditions. Patients allergic to antibiotics or with any systemic problems were excluded from this study. Following surgery, 82 surgical cases were prescribed antibiotics (group 1), and 138 surgical cases were not prescribed antibiotics (group 2). Periodontal surgical techniques employed included flap surgery, osseous surgery, gingivectomy/gingivoplasty, soft tissue grafting, and tooth resection. Postoperative infection was defined as progressively severe pain, pus exudate, local swelling, and lymphadenopathy. The degree of wound redness and swelling was also recorded. The mean age in group 1 was 38.3 +/- 13.8 and was 38.9 +/- 14.6 years in group 2 (p = 0.78). The total occurrence of postoperative infection was 3.6% (8/220), including 3.7% (3/82) in the group with antibiotics and 3.6% (5/138) in the group without antibiotics. There was no statistical difference in the incidence of postoperative infection between the two groups (Zc = -0.36, p = 0.72). Based on the results of this prospective study, we conclude that the routine prescription of antibiotics is not necessary following periodontal surgery using aseptic surgical techniques.

Adult↗
PubMed1993

Oral health conditions among people visiting a medical center for health checkups.

The purpose of this study was to evaluate the oral health conditions of subjects in a southern Taiwan health checkup program. One half of the examinees were selected randomly for oral examination during a two-year period. There were 537 subjects, including 286 men and 251 women with mean ages of 49.7 +/- 13.5 years and 50.2 +/- 12.1 years, respectively. Oral examinations included periodontal condition and existence of dental caries. The periodontal treatment needs of all examinees were evaluated using the Community Periodontal Index of Treatment Needs system and the World Health Organization periodontal probe. Dental caries examination was performed by the visual-tactile method with a mouth mirror and explorer. No radiographs were taken. All clinical evaluations were performed by the first author, who has experience in all of the indices. The results showed that only 0.7% of the subjects had no need of periodontal treatment, 6.7% had bleeding after gentle probing, and 75.2% presented with calculus, overhanging restorations, or pockets of 4 or 5 mm. The remaining 17.3% had pocket depths of 6 mm or deeper. There was no statistically significant difference between males and females in periodontal treatment needs and the mean number of decayed teeth (D). According to this hospital-based observation, most of the people in the health checkup program were in need of periodontal treatment, including oral hygiene instruction, prophylaxis and root planing. Approximately one-fifth of the subjects needed complex periodontal treatment; there were no differences in the treatment needs of males and females.(ABSTRACT TRUNCATED AT 250 WORDS)

Academic Medical Centers↗
PubMed1992

Experimental chemotherapy for xenograft cell lines of human bile duct and gall bladder cancers in nude mice.

Most biliary tract cancers are advanced and inoperable when first diagnosed. Even if surgery can be performed, the postsurgical prognosis of these diseases is poor. In the present study, we investigated effective chemotherapies for a human bile duct cancer xenograft cell line (undifferentiated carcinoma, BDC-SN) and a gall bladder cancer xenograft cell line (well-differentiated adenocarcinoma, GBC-GN), which were transplanted into nude mice. Eight anticancer agents (CDDP, 5-FU, VDS, MMC, ADR, EPIR, CQ, and VP-16) and their various combinations were evaluated at 2-4 times the clinical dose. When used singly, CDDP, 5-FU, and VDS were effective against BDC-SN, and only CDDP was effective against GBC-GN. Among the various 2-agent combinations, CDDP + 5-FU was the most effective against both BDC-SN and GBC-GN. However, 3-agent combinations consisting of CDDP + 5-FU + another agent were less effective than the CDDP + 5-FU double regimen and caused significant loss of weight as well as high mortality. These results suggest that CDDP + 5-FU may be the most useful regimen against biliary tract cancers in clinical application.

Adenocarcinoma↗
PubMed1992

Comparative effects of a recombinant and a mutein type of granulocyte colony stimulating factor on the growth of Meth-A fibrosarcoma with 5-fluorouracil chemotherapy.

The present study was designed to evaluate the effects of a recombinant human G-CSF (rhG-CSF) and a mutein G-CSF (KW-2228) on leucopenia and tumor growth in mice treated with 5-fluorouracil (5-FU). In normal mice, the number of leucocytes (white blood cell, WBC) reached the peak 12 hours after a single injection of either type of G-CSF and decreased to the normal level after 24 hours. Daily administration induced a continuous increase in the WBC count, however, administrations at intervals did not. Meth-A fibrosarcoma was subcutaneously inoculated into the backs of syngeneic BALB/c mice. The mice were treated with 5-FU alone or with G-CSFs. Chemotherapy with 5-FU alone resulted in leucopenia and an insignificant inhibition of tumor growth. The conjunctive administration of G-CSFs with 5-FU resulted in a significantly augmented inhibition of tumour growth, and leukopenia was not seen. This augmenting effect was more prominent with KW-2228. These results suggest that in 5-FU chemotherapy G-CSFs may be beneficial in restoring the number of leucocytes from leucopenic state and in augmenting the tumor inhibitory effect. Furthermore, KW-2228 may be more beneficial than the natural type rhG-CSF.

Amino Acid Sequence↗
PubMed1992

Immunomodulation by orally administered protein-bound polysaccharide PSK in patients with gastrointestinal cancer.

The present study was designed to assess the effects of the protein-bound polysaccharide PSK on the immunological status of patients with gastrointestinal cancer. Twenty-nine gastric and 18 colorectal cancer patients were randomly assigned to either the control or PSK group. Patients in the PSK group were given 3.0 g of PSK orally before surgery, either daily or every other day. Patients in the control group received no PSK. The data of peripheral blood lymphocytes (PBL) were compared before and after administration of PSK, and those of the regional node lymphocytes (RNL) were compared between the control and the PSK group. The results indicate that the effects of PSK were significantly influenced by the duration of administration, but not by the frequency of administration. In the patients belonging to the short term PSK group (administration less than 14 days), the response of the PBL to PSK and Con A become significantly stronger compared to before the administration of PSK, whereas the cytotoxicity against K562 and KATO-3, and the proportion of CD16+ cells increased significantly in those patients belonging to the long term PSK group (greater than or equal to 14 days). In addition, the proportion of CD9 + 11b + suppressor T cells decreased in the RNL of the short term PSK group, whereas the proportion of CD4 + Leu8 - helper T cells in the RNL increased in the long term PSK group. These results suggest that the oral administration of PSK leads to the suppression of suppressor cells in the RNL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adjuvants, Immunologic↗
PubMed1992

Cocaine-induced respiratory depression and seizures are synergistic mechanisms of cocaine-induced death in rats.

STUDY OBJECTIVE: To determine if respiratory depression is an important mechanism of cocaine-induced death in conscious rats. DESIGN: Male Sprague-Dawley rats weighing between 200 and 300 g and fitted with cortical electrodes were pretreated intraperitoneally with either saline (vehicle), MK-801, or valproic acid for 30 minutes before challenge with 70 mg/kg IP cocaine followed by spontaneous breathing or mechanical ventilation after acute tracheostomy. Behavior, seizures, death, EEGs, and ECGs were observed and measured. MEASUREMENTS AND MAIN RESULTS: In group 1, animals received saline followed by cocaine. The incidence rates of seizures and death were 92% and 83%, respectively. Group 2 received saline followed by cocaine and then were ventilated mechanically through an acute tracheostomy after respiratory arrest (late mechanical ventilation). This group experienced seizures in 100% and death in 67% of animals. Group 3 also received saline followed by cocaine but were ventilated mechanically immediately after the first seizures (early mechanical ventilation). They had experienced seizures in 100% and death in 30%, the latter being significantly (P less than .025) reduced compared with group 1. In group 4, an anticonvulsant (1 mg/kg MK-801) was given before cocaine challenge, resulting in seizures in 10% (P less than .002 compared with group 1) and death in 90%. Group 5 received MK-801 followed by cocaine and then were ventilated mechanically after respiratory arrest (late mechanical ventilation). They experienced seizures in 20% (P less than .002 compared with group 1), and no animals in this group died (P less than .002 compared with group 1 or 4). Group 6 received an anticonvulsant (400 mg/kg valproic acid), followed by cocaine. This resulted in seizures in 20% (P less than .002 compared with group 1) and death in 90%. Group 7 received valproic acid followed by cocaine and then were ventilated mechanically (late mechanical ventilation). They experienced seizures in 30% (P less than .002 compared with group 1), and all animals survived (P less than .002 compared with group 1 or 6). CONCLUSION: Early mechanical ventilation reduces cocaine toxicity. Control of seizure activity with specific anticonvulsants allows delayed mechanical ventilation to protect against cocaine toxicity. This suggests that respiratory depression in conjunction with seizure activity plays a major role in the mechanisms of cocaine-induced death in this model.

Animals↗
PubMed1992

Primary structure of an inactive mutant of phospholipase A2 in the venom of Bungarus fasciatus (banded krait).

From the acidic components of Bungarus fasciatus venom, a very small amount (0.16%) of a novel phospholipase A2 was obtained. Both neurotoxicity and enzyme activity were found to be lacking. Amino acid sequence study showed that it has a normal backbone of group I snake venom phospholipase A2 with 118 amino acid residues. The lack of enzyme activity was attributed to its mutation of the indispensable Asp residue to an Ala residue, i.e., the usual His-Asp47 turned out to be His-Ala47. This is the eighth isoform of phospholipase A2 found from the venom of Bungarus fasciatus. Examination of structural homology with three other isoforms revealed 66% similarity at most.

Amino Acid Sequence↗
PubMed1992

The effect of morphine and naloxone on cocaine toxicity.

The effect of morphine and naloxone on acute cocaine toxicity was studied. Male Sprague-Dawley rats were pretreated intraperitoneally (ip) with saline, morphine sulfate 25 mg/kg, or naloxone 1.0 mg/kg 15 minutes prior to challenge by cocaine. After pretreatment, each group was challenged with one of three doses of cocaine (35, 50, or 75 mg/kg ip). Each of the nine drug combinations was tested on at least 10 animals. Animals were observed for behavior, seizures, and death. The animals pretreated with saline and challenged with cocaine (35, 50, or 75 mg/kg) had seizure incidences of 0%, 40%, and 100%, respectively, after increasing doses. Pretreatment with morphine resulted in cocaine-induced seizures of 20%, 80% and 100%, respectively (p less than or equal to 0.05 with cocaine 35 and 50 mg/kg). Time to seizures in these groups did not differ significantly compared to the saline groups. Pretreatment with naloxone resulted in cocaine-induced seizures of 0%, 50%, and 60% (p less than or equal to 0.05 at the 75 mg/kg dose). The incidence of death was significantly increased by pretreatment with morphine in animals that received cocaine 50 or 75 mg/kg. The time to death was not significantly different compared to saline controls. The death rate in naloxone pretreated animals was not significantly different from the saline groups. In additional studies, high-dose naloxone pretreatment (10 mg/kg) also failed to provide protection from acute cocaine toxicity. In conclusion, cocaine toxicity is potentiated by morphine and does not appear to be altered by naloxone.

Animals↗
PubMed1992

A comparative study of the antitumor activities of 5'-deoxy-5-fluorouridine and its prodrug trimethoxybenzoyl-5'-deoxy-5-fluorocytidine (Ro09-1390) on human digestive organ cancer xenograft lines transplanted into nude mice.

5'-Deoxy-5-fluorouridine (5'-DFUR) is one of the oral fluoropyrimidines widely used in the treatment of gastric, colorectal and breast cancers in Japan. 5'-DFUR is converted to 5-fluorouracil by pyrimidine nucleoside phosphorylase in the tumor. 5'-DFUR has toxic effects on the intestine and may cause severe diarrhea. Trimethoxybenzoyl-5'deoxy-5-fluorocytidine (Ro09-1390) is a prodrug of 5'-DFUR, which was developed to reduce the intestinal toxicity of 5'-DFUR. The present study was designed to assess the antitumor activity and spectrum of Ro09-1390, and to compare its efficacy with that of 5'-DFUR. Six digestive organ cancer xenograft lines (two gastric, one esophageal, one colorectal, one gall bladder and one bile duct cancers) were s.c. transplanted into nude mice. The agents were orally administered daily for 14 days at doses of 0.08-0.64 mmol/kg (1-8 times the maximal clinical dose of 5'-DFUR). Both 5'-DFUR and Ro09-1390 significantly inhibited the growth of two gastric cancer lines, and the IC50's for Ro09-1390 in both lines were lower than the respective values for 5'-DFUR. The esophageal, colorectal, gall bladder and bile duct cancer lines, however, were resistant to both agents. 5'-DFUR at 0.64 mmol/kg significantly inhibited the growth of these cancers, but with high mortality, and most mice receiving this dose died within 14 days after the start of therapy, suffering from severe diarrhea and body weight loss. Ro09-1390 at the same dose resulted in low mortality, but evidenced similarly low antitumor activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Use of a replica-plate assay for the rapid assessment of salivary protein-bacteria interactions.

A replica-plate assay was used to screen for the interaction of salivary molecules with dental plaque bacteria. Bacterial colonies cultured from supragingival plaque on sheep-blood (SB) agar were replica-plated onto nitrocellulose membranes overlaying SB or mitis-salivarius agar. Membranes with attached colonies were removed and incubated with 125I-amylase or 125I-proline-rich glycoprotein (PRG). Positive interactions were detected by autoradiography. Only strains of Streptococcus gordonii and Actinomyces viscosus bound amylase, and strains of A. viscosus bound PRG. The results suggest that amylase and PRG bind to selected species of aerobic dental plaque bacteria.

Actinomyces↗
PubMed1992

Effect of gels containing stannous fluoride on oral bacteria--an in vitro study.

The purposes of this investigation were to evaluate and compare the antimicrobial effect of (1) twelve 0.4 per cent stannous fluoride (SnF2) commercial products and (2) different concentrations of SnF2 (range = 0.02 to 3.28 per cent). The antibacterial inhibitory effect of various SnF2 gels was evaluated as to their effectiveness against oral plaque bacteria including strains of S. mutans, S. sanguis, S. sobrinus, A. viscosus, A. actinomycetemcomitans, and B. intermedius. When twelve different commercial preparations of 0.4 per cent SnF2 were compared for inhibitory effect on plaque bacteria, several of the SnF2 preparations were significantly more effective in inhibiting oral bacteria (p < 0.05). With increasing concentration of SnF2, there was a comparable increase in the inhibitory effect on the oral bacteria tested (r2 ranged from 0.867 to 0.996). SnF2 at a concentration of 0.4 per cent had a similar antibacterial effect to 0.12 per cent chlorhexidine. This in vitro study demonstrated that certain SnF2 products are highly effective in inhibiting the growth of bacteria often found in plaque, and this inhibitory effect is directly related to the concentration of the SnF2.

Actinomyces viscosus↗