[Effect of PPAR-γ agonist pioglitazone on the prolifeiration of malignant nesothelionma cells induced by HMGB1].

Objective: To investigate the effect and mechanism of PPAR-γ agonist Pioglitazone (PGZ) on the proliferation of malignant mesothelioma (MM) cells. Methods: In December 2019, MM cell lines MSTO-211H and NCI-H2452 were incubated with different final concentrations of PGZ (0, 10, 50, 100, 150, and 200 µmol/L) for different periods of time (24 h, 48 h, and 72 h) , and then the cell proliferation level was detected by CCK8 assay. After given various final concentration of PGZ (0, 10, 50, 100, 150, 200 µmol/L) the for 72 hours, the changes of number and morphology of MM cells were observed under an inverted microscope. The expressions of PPAR-γ and HMGB1 mRNA were determined by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) after treatment of MM cells with PGZ of 0, 10, 50, 100 µmol/L for 72 h. The MM cells were treated with PGZ at concentration of 0, 100 µmol/L for 72 h, and the protein expressions of HMGB1 were examined using Western blotting and immunofluorescence; the protein expressions of Ki67 were assessed by immunohistochemistry. Results: The cell viability rate of MM cells was decreased after treated with PGZ (P<0.05) . Cell number in PGZ-treated group was significantly less than that in control group and morphology changes were observed under light microscope. QRT-PCR results revealed significantly increased PPAR-γ mRNA expression in the PGZ-treated group compared to the control group (P<0.05) . There was a significant decrease in the mRNA expression level of HMGB1 in the PGZ-treated group (100 µmol/L) as compared to the control group in MSTO-211H (P<0.05) ; however, the expression level of HMGB1 in NCI-H2452 was an increase or no significant differences (P>0.05) . Western blotting and immunofluorescence results showed that the protein expression of HMGB1 was reduced in the PGZ-treated group compared with the control group in MSTO-211H (P<0.05) , but the protein expression of that in NCI-H2452 was no significant differences (P>0.05) . Immunohistochemistry results showed increased expression of proliferation marker Ki-67. Conclusion: Pioglitazone suppresses the proliferation of MM cells through inhibition of HMGB1 by the activation of PPAR-γ.

Aspirin Blocks Orthodontic Relapse via Inhibition of CD4+ T Lymphocytes.

Immunologic response plays an important role in orthodontic tooth movement (OTM) and relapse. Nonsteroidal anti-inflammatory drugs, such as aspirin, affect immune cells and clinical orthodontic treatment. However, the mechanisms by which nonsteroidal anti-inflammatory drugs regulate immune cells to affect orthodontic relapse are unclear. In this study, male Sprague-Dawley rats were grouped as relapse and relapse + aspirin for 10 d after 14 d of OTM. Silicone impressions of the rats' maxillary dentitions were obtained to record the distance of OTM at the indicated time point. CD4+ T lymphocytes in spleen were examined by flow cytometry. Serum levels of type 1 T-helper (Th1) cell-associated cytokines tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) were determined through enzyme-linked immunosorbent assay. The effects of aspirin on CD4+ T and Th1 cells were also analyzed in vitro. Aspirin treatment significantly reduced the relapse rate. More interestingly, injection of CD25 neutralizing antibody basiliximab or TNF-α inhibitor etanercept can significantly reduce the relapse rate as well. Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force-induced secretion of TNF-α and IFN-γ in serum and the expression of TNF-α and IFN-γ in periodontal ligament during relapse. Furthermore, aspirin treatment in vitro significantly repressed the differentiation of CD4+ T and Th1 cells. Overall, results indicated that aspirin treatment can block orthodontic relapse by regulating Th1 cells.

PTEN activation through K163 acetylation by inhibiting HDAC6 contributes to tumour inhibition.

Phosphatase and tensin homologue deleted on chromosome 10 (PTEN), an important tumour-suppressor gene, is mutated, downregulated or dysfunctional in many tumours. The phosphatase activity of PTEN depends on membrane translocation (activation). As promising anti-cancer agents, histone deacetylase (HDAC) inhibitors, particularly trichostatin A (TSA), can promote PTEN membrane translocation, but the underlying mechanism remains unknown. In this study, we revealed that non-selective HDAC inhibitors, namely, TSA or suberoylanilide hydroxamic acid (SAHA), induced PTEN membrane translocation through PTEN acetylation at K163 by inhibiting HDAC6. K163 acetylation inhibited the interaction of the PTEN C-tail with the remaining part of PTEN, resulting in PTEN membrane translocation. Overexpression of wild-type PTEN, but not K163-mutated PTEN, facilitated the inhibition of cell proliferation, migration and invasion, as well as xenograft tumour growth, induced by SAHA or tubastatin A, an HDAC6-specific inhibitor. These results indicated that PTEN activation by inhibiting HDAC6 significantly contributed to tumour inhibition. Therefore, non-selective HDAC or HDAC6-specific inhibitors may be more clinically suitable to treat tumours without PTEN mutations or deletions.

Association of GDF5, SMAD3 and RUNX2 polymorphisms with temporomandibular joint osteoarthritis in female Han Chinese.

Temporomandibular joint osteoarthritis (TMJOA) is a complex disease and has a strong genetic component in its pathogenesis. Experimental evidence suggests the involvement of biological pathway in the disease. This case-control study was designed to investigate whether five common single nucleotide polymorphisms (SNPs) in GDF5, SMAD3, RUNX2, TGFß1 and CHST11, respectively, are associated with TMJOA in female Han Chinese patients. A total of 240 participants were evaluated comprising 114 female patients diagnosed with TMJOA based on Research Diagnostic Criteria for Temporomandibular Disorders and 126 healthy female controls. The SNPs of the five genes in the genomic DNA were examined by sequencing, and their allelic, genotypic and carriage rate frequency distributions, as well as the triple combination of the risk genotypes, were analysed using the logistic regression model. The SNP in GDF5 or SMAD3 showed significant association with TMJOA, a relatively weak association was observed in RUNX2. In the triple combinational analysis, the risk of TMJOA grew 5·09 times in the patients with five or six risk alleles (P < 0·01). This is the first study to evaluate the association of GDF5, SMAD3, RUNX2, TGFß1 and CHST11 with TMJOA in female Han Chinese. Our study suggests that the SNPs of genes related to TGFß family might contribute to the risk of TMJOA.

Radiofrequency ablation guided by contrast-enhanced ultrasound for hepatic malignancies: preliminary results.

AIM: To evaluate whether contrast-enhanced ultrasound (CEUS)-guided radiofrequency ablation (RFA) can be performed effectively in small hepatic malignancies that are invisible or poorly visualized at traditional grey-scale ultrasonography (US). MATERIALS AND METHODS: The institutional ethics committee approved the study, and all patients provided written informed consent before their enrolment. The study focused on 55 patients (43 men, 12 women, age 57.4 ± 10.9 years) with 60 hepatic lesions from May 2010 to March 2011. All lesions were treated with multipolar radiofrequency ablation (RFA). During the RFA procedure, with the injection of ultrasound contrast agent (sulphur hexafluoride; SonoVue, Bracco Imaging Spa, Milan, Italy), RFA was conducted under CEUS guidance when the optimal depiction of a lesion was obtained. Artificial pleural effusions were used in those cases obstructed by the lungs. Twenty-four hours after RFA, contrast-enhanced MRI was used as the reference standard to evaluate the primary effectiveness rate and complete tumour necrosis. The follow-up time was 12-24 months (median 15 months). RESULTS: Among 60 hepatic malignancies, CEUS detected 57 lesions (95%), which was higher than that at US (26.6%). Artificial pleural effusions were performed in three cases, resulting in the detection of three additional lesions. The insertion of RFA electrodes was monitored by CEUS in all lesions. Immediately after RFA, complete tumour necrosis were achieved in all 60 lesions as apparent at MRI, for a primary effectiveness rate of 100%. CONCLUSION: CEUS-guided RFA is a promising technique for targeting and improving the efficiency of treatment of hepatic malignancies.

Estrogen aggravates iodoacetate-induced temporomandibular joint osteoarthritis.

Temporomandibular joint osteoarthritis (TMJOA) is clinically characterized by female preponderance, with a female-to-male ratio of more than 2:1; however, the underlying mechanism remains obscure. We examined the effects of estrogen on TMJOA induced by monosodium iodoacetate. Female rats were randomly and equally divided into 5 groups: control, sham-ovariectomized, and ovariectomized rats treated, respectively, with 17ß-estradiol (E2) at doses of 0 µg, 20 µg, and 80 µg/day until the end of the experiment. After induction of TMJOA, TMJs were evaluated by histopathology and microCT, and the expression of Fas, FasL, caspase 3, and caspase 8 was evaluated by real-time polymerase chain-reaction or immunohistochemistry. Another 5 groups of female rats were used to evaluate the effect of estrogen receptor antagonist ICI 182780 on E2 effects on TMJOA, when injected intraperitoneally into the control, sham-ovariectomized, and 80-µg-E2-treated groups. We found that E2 potentiated cartilage degradation and subchondral bone erosion in iodoacetate-induced TMJOA. E2 also potentiated mRNA expression of Fas, FasL, caspase 3, and caspase 8 in the condylar cartilage. Moreover, the estrogen receptor antagonist partially blocked E2 effects on TMJOA. These findings suggest that E2 could aggravate TMJOA, which may be an important mechanism underlying the sexual dimorphism of TMJOA.

Decreased osteogenesis in stromal cells from radiolucent zone of human TMJ ankylosis.

We previously hypothesized that the development of traumatic temporomandibular joint (TMJ) ankylosis was similar to that of hypertrophic non-union. Besides similarities in etiology, hypertrophic bone stumps, and long-term development, the radiolucent zone, frequently located in the ankylosed bone, is another common feature. In this study, we demonstrated that the radiolucent zone also contained multilineage potential cells (RZs, radiolucent-zone-related cells) as the non-union tissues. RZs were characterized and compared with mandibular bone marrow stem cells (BMSCs) by analysis of MSC-related markers, colony-forming-unit assays, multipotential differentiation assays, alkaline phosphatase (ALP) activity assays, and cell transplantation in vivo. Both cell types were positive for CD105, CD166, and Stro-1 expression, negative for CD34 and CD45 expression, and exhibited osteogenic, adipogenic, and chondrogenic differentiation potentials. However, compared with mandibular BMSCs, RZs showed lower colony-forming-unit abilities and proliferation rates. The mineralization and bone-forming ability of RZs was weaker than that of mandibular BMSCs, with Runx2 and ALP mRNA expression and ALP activity significantly lower in RZs. All these results suggest that RZs possess the properties of MSCs but lower proliferation and osteogenic differentiation capacity similar to that of stromal cells in hypertrophic non-union tissues.

TGF-beta1 promotes migration and invasion of salivary adenoid cystic carcinoma.

Salivary adenoid cystic carcinoma (SACC) is one of the most common subtypes of salivary gland carcinomas and frequently metastasizes to distant organs. However, little is known about the molecular mechanisms that promote SACC metastasis. In this study, we report that transforming growth factor (TGF)-ß1 was highly expressed in the highly metastatic SACC-LM cell line as compared with its parental low-metastatic SACC-83 cell line. Exogenous addition of TGF-ß1 induced Smad2 phosphorylation and promoted the migration and invasion of SACC-83 cells. Consistently, the inhibition of endogenous TGF-ß1 signaling in SACC-LM cells by an inhibitor specific to the type I TGF-ß1 receptor (TßRI) suppressed cell migration and invasion. Moreover, we found that TGF-ß1 expression was significantly increased in human primary SACC samples with metastasis. Taken together, our results suggest that TGF-ß1 may play a crucial role in SACC metastasis.

Flagella are virulence determinants of Burkholderia pseudomallei.

Burkholderia pseudomallei, a facultatively intracellular pathogen, is a flagellated and motile gram-negative bacterium and is the causative agent of melioidosis in humans. Flagella are commonly recognized as important virulence determinants expressed by bacterial pathogens since the motility phenotype imparted by these organelles often correlates with the ability of an organism to cause disease. We used a virulent isolate of B. pseudomallei, KHW, to construct an isogenic deletion mutant with a mutation in the flagellin gene (fliC) by gene replacement transposon mutagenesis. The KHWDeltafliCKm mutant was aflagellate and nonmotile in semisolid agar. The isogenic KHWDeltafliCKm mutant was not impaired in terms of the ability to invade and replicate in cultured human lung cells compared with the wild type. It was also equally virulent in slow-killing assays involving Caenorhabditis elegans, but it was avirulent during intranasal infection of BALB/c mice. Very few bacteria, if any, were isolated from the lungs and spleens of KHWDeltafliCKm-infected mice. In contrast, the bacterial loads in the lungs and spleens were similar in mice infected with KHW and in mice infected with the complemented mutant, KHWDeltafliCKm/pUCP28TfliC. Unlike the Syrian hamster or diabetic rat models of infection, the B. pseudomallei flagellin was also a virulence factor during intraperitoneal infection of BALB/c mice. In this study, all animals infected with KHWDeltafliCKm remained healthy and did not succumb to disease regardless of the route of infection. The flagellum is therefore an important and necessary virulence determinant of B. pseudomallei during intranasal and intraperitoneal infection of mice.

Fas-dependent, activation-induced cell death of gammadelta cells.

Activated gammadelta T cells undergo apoptosis upon restimulation of their T cell receptor (TCR)/CD3 complex. We demonstrate that in these cells, the activation-induced cell death (AICD) is mediated by Fas and Fas ligand (FasL) interaction. The activated gammadelta T cells are prone to AICD initiated by exposure to mitogens, anti-TCR/CD3 antibodies, as well as specific antigens such as Daudi cells or ethylpyrophosphate (Etpp). Cells that have been activated twice, and consequently more susceptible to AICD than primary cells, display augmented tyrosine phosphorylation in comparison with control cells. These studies outline a mechanism that may regulate gammadelta T cell activities in immune responses and limit the expansion of activated T cells repeatedly exposed to antigens.

Immunomodulating activity of mycobacterial heat shock protein 65 in tumor cells.

In recent years, heat shock proteins have been shown to be effective in enhancing the immunogenicity of tumors. In this study, we examined the effect of mycobacterial hsp65 gene transfection in a non-immunogenic and aggressive tumor cell-line in order to understand the factors that could contribute to the increase in immunogenicity mediated by Hsp65. The transfected cells were found to have indeed lost their tumorigenenicity and increased their immunogenicity. Tumor-specific cytotoxic T cells were present only in mice immunized with the Hsp65-expressing cells. Furthermore, endogenous Hsp70 was significantly increased in irradiated Hsp65-expressing cells and recombinant Hsp65 protein was able to stimulate the mRNA expression of various T helper 1 (Th1) and pro-inflammatory cytokines in splenocyte cultures, as well as a modest expansion of CD4 T cells. These results provide further evidence of the immunomodulating properties of Hsp65, which could be exploited for the treatment of cancer.

Differential susceptibility of naïve and activated human gammadelta T cells to activation-induced cell death by T-cell receptor cross-linking.

BACKGROUND: T cells undergo activation-induced cell death (AICD) through repeated stimulation of their T cell receptors (TCRs). Activated human gammadelta T cells were found to die by apoptosis when their TCRs were cross-linked by antibodies, whereas naïve gammadelta T cells freshly isolated from blood did not. Therefore, we investigated the factors that could contribute to this differential susceptibility. MATERIALS AND METHODS: Gammadelta T cells were isolated from the peripheral blood of healthy human volunteers and their TCRs were cross-linked either directly (naïve) or after an in vitro incubation of 11 days (activated). Their cell cycle profiles, cytokine, Fas and FasL mRNA messages, and surface expression of Fas and FasL were determined. RESULTS: The naïve cells were cycling while the activated T cells exited from the G1 to subG1 phase upon TCR cross-linking. IL-2 and IL-4 mRNAs and surface expression of FasL were detected only in activated T cells in the time period examined. In addition, cFLIP mRNA expression was found only in naïve gammadelta T cells and activated T cells treated with cyclosporin A (CsA), which inhibited AICD in the activated T cells. CsA also downregulated the surface expression of FasL in activated T cells. CONCLUSIONS: The differential expression of cytokines, apoptotic inducers and inhibitors provide the basis for the differential susceptibility of naïve and activated gammadelta T cells to AICD upon TCR cross-linking. This contributes to our understanding of the regulation and maintenance of gammadelta T-cell homeostasis, which would be important in many infectious as well as autoimmune diseases, where gammadelta T cells have been implicated.

Molecular mechanism of apoptosis induced by ricin in HeLa cells.

AIM: To study the morphological changes and molecular mechanism of HeLa cell apoptosis induced by ricin. METHODS: HeLa cells were coincubated with ricin 0.05 mumol.L-1 for 1, 2, 3, 6, 12, 18, and 24 h, then scanning electron microscopy (SEM), transmission electron microscopy (TEM), Western blot cell cycle, cell cytotoxicity, and cell viability were assayed. RESULTS: The typical apoptosis was induced by ricin 0.05 mumol.L-1 and necrotic cells increased after being cultured with ricin 0.05 mumol.L-1 for more than 12 h. The apoptotic cells mainly showed cytoplasmic membrane blebbing, chromatin condensation and fragmentation, and crescentic nuclear and membrane bound apoptotic bodies formation. No detectable levels of p53, Bax, Bcl-2 and the subunit p20 of interleukin-1 beta-converting enzyme (ICE) were found by Western blot, but the active subunit p17 of 32-kDa putative cysteine protease (CPP32) was detected at 3, 6, and 9 h after ricin treatment. The activity of CPP32 in HeLa cells increased 4 to 5 folds after being treated with ricin 0.05 mumol.L-1 and reached the peak at 6 h of treatment. There was no significant difference of ICE activity between the ricin treated cells and control cells. The percentage of G2/M cells increased from 13.9% +/- 0.5% to 33.2% +/- 0.5% after 24 h of ricin 0.05 mumol.L-1 treatment. CONCLUSION: CPP32 but not ICE was involved in the ricin-induced apoptosis in HeLa cells. Ricin 0.05 mumol.L-1 had no effect on the G0/G1 phase of cell cycle, but induced G2/M arrest.

Antitumour immunity of Bacillus Calmette-Guerin and interferon alpha in murine bladder cancer.

Intravesical Bacillus Calmette-Guerin (BCG) immunotherapy is currently the optimal choice for aggressive superficial bladder cancer, with a 70% response rate. This study investigated whether the antitumour response elicited by BCG could be improved by the addition of recombinant interferon alpha (IFN alpha) in the subcutaneous murine MB49 bladder tumour model. The combination of BCG and IFN alpha had superior and earlier antitumour activity than BCG alone for MB49 cells in culture. A total of 14/15 BCG plus interferon-treated mice and 8/16 BCG-treated mice became tumour free after treatment. BCG or the combination treatment significantly raised the T-helper 1 (Th1) cytokine IFN gamma levels compared with levels in all other groups. Whilst BCG therapy alone increased CD4+ and CD8+ populations in spleens, the combination of BCG and IFN alpha also increased alpha beta+ T cells significantly. Our results suggest that the combination of BCG and IFN alpha may represent a more efficacious therapeutic than BCG alone for superficial bladder cancer.

Distribution of epstein-barr virus antigenic sites on the carboxyl terminal end of ribonucleotide reductase against nasopharyngeal carcinoma serum antibodies using an immunoabsorption method.

In an attempt to clone and express proteins from the Epstein-Barr virus (EBV) cDNA library to be used as antigens in an enzyme-linked immunosorbent assay (ELISA) format to test against the antibodies found in the sera of nasopharyngeal carcinoma (NPC) patients, we have isolated and characterized three clones. All three clones expressed the same polypeptides of different lengths, which belong to the carboxyl terminal end of the large subunit of ribonucleotide reductase (RR) of the EBV genome. All three clones were found to be immunogenic and could be used in an IgA and IgG ELISA against the NPC sera with various degrees of sensitivity and specificity. Because the clones varied in length, this difference provides a simple system to determine where most of the antibody epitopes lies on the protein. We designed an immunoabsorption assay and a mathematical model to help map the segment of the polypeptide most immunogenic to 43 NPC patients. Results were unexpected: 77% of the patients were most immunogenic to region z, which was the smallest fragment among the three fragments studied. Fragment z was only 33 amino acids in length. Only 14% and 19% of patients showed the most immunogenic region in segment x and y, respectively. This variation could be due to major histocompatibility complex antigens. The patients could be divided into three groups based on the immunoabsorption assays, in which each group responded to a different immunodominant segment in the RR antigen. The largest group responded to an immunodominant segment, which was only 33 amino acids long. This domain was coded for by the gene fragment from nucleotide 78,129 to nucleotide 78,227 of the EBV genome. This segment of the protein would be suitable for further epitope mapping studies.

Evaluation of lymphocytic responses after treatment with Bacillus Calmette-Guerin and interferon-alpha 2b for superficial bladder cancer.

Bladder wash-derived lymphocytes from superficial bladder cancer patients involved in high dose BCG, low dose BCG, and low dose BCG with IFN-alpha treatments were examined. We found an increasing trend in the percentage of CD3 T cells with each weekly intravesical instillation and the proportion of CD3 T cells expressing the gammadelta T cell receptor was significantly higher in patients receiving standard dose BCG than those receiving low dose BCG or low dose BCG plus IFN-alpha. Most patients had a predominance of CD4 T cells, while some had more CD8 T cells. The CD4/CD8 ratio did not vary much during the instillations. Surprisingly, both patients and normal control individuals had high percentages of CD69- and CD45RO-positive lymphocytes in the bladder wash and this was not reflected in lymphocytes from peripheral blood collected in parallel. We found no differences in lymphocyte phenotypes, cytokine production, and clinical outcome in the patients from three arms. This may reflect that the qualitative and quantitative immune responses elicited from the three treatments are similar. However, the lymphokine-activated killing ability of peripheral blood lymphocytes against allogeneic cell-lines from the cancer patients was depressed compared to normal individuals and the cytotoxicity appeared to be enhanced after intravesical treatment.

Mechanisms of simian gamma delta T cell cytotoxicity against tumor and immunodeficiency virus-infected cells.

The mechanisms of cytotoxic killing of various tumor cell lines and immunodeficiency virus-infected T cell lines by simian gamma delta T cells were examined. The lysis of the majority of the target cell lines by gamma delta effectors was calcium-dependent, indicating that cytotoxicity is mediated by the perforin/granzyme pathway rather than the Fas-FasL pathway, with the exception of Jurkat cells. The gamma delta T cells were able to suppress SIV replication as measured by the p27 ELISA and the suppression was contact-dependent. We further determined that the target cells were induced to undergo apoptosis by the gamma delta T cell effectors. These results contribute to our understanding of the function of simian gamma delta T cells and their similarities to human gamma delta T cells, and extend our knowledge on the cytotoxic mechanisms employed by gamma delta T cells in general.

Color-Doppler Ultrasound-assisted endoscopic neurosurgery for intracerebral hemorrhage.

BACKGROUND: Over the past few years, the use of endoscopy in neurosurgery has gradually gained importance. In this study we described the performance of Color Doppler Ultrasound (CDU)-guided endoscopic neurosurgery in ten patients with intracerebral hemorrhage. The completeness of hematoma evacuation was also evaluated. METHODS: CDU, resectoscope, cutting loops, biopsy forcep, and the irrigation and suction device were the main instruments used in treating intracerebral hematoma. The CDU probe was utilized to locate the exact position of the hematoma and to provide direct visual control of the operation. The cutting loops and biopsy forcep were applied to morcellate and fragment the hematoma. Next, the fragmented hematoma was aspirated by a suction and irrigation device. CDU was then re-used to verify the completeness of hematoma resection and hemostasis as well as evaluate the position of midline shifting. RESULTS: The completeness of hematoma evacuation in our patient series was over 90% in three patients, over 50% in five patients, and less than 50% in two patients. One patient showed signs of rebleeding two days post-operatively and underwent conventional craniotomy. CONCLUSIONS: This endoscopic neurosurgical procedure caused less trauma around and along the route to the hematoma, and inflicted less damage to healthy brain tissue. Sonography, especially CDU, is quite helpful in the localization of hematoma and evaluation of intra- or post-operative bleeding. The operation time was also significantly shortened as compared to conventional craniotomy, thereby reducing the risk of operation.

Gamma delta T cells in rhesus monkeys and their response to simian immunodeficiency virus (SIV) infection.

Recent reports of the increase in peripheral blood gamma delta T cells in HIV+ patients prompted us to examine the gamma delta T cell system in rhesus monkeys (Macaca mulatta) and the responses of these cells to SIV infection. Our results reveal differences in the gamma delta T cell subset composition and their expression of CD8 in the peripheral blood of monkeys and humans. The outgrowth of simian gamma delta T cells in response to Daudi cells is similar to that in humans, but the exposure to IL-2 stimulates preferentially the simian V delta 1 subset rather than the V gamma 9/V delta 2 subset as found in humans. Upon SIV infection of the monkeys, we observed a transient increase of the percentage of total gamma delta T cell and the V gamma 9 subset. gamma delta T cells from infected animals also express more activation markers such as CD69, CD44 and the memory marker CD45RO. However, they respond to a lesser degree to Daudi or IL-2 stimulation in the outgrowth experiments compared with uninfected animals, although the subset composition of total gamma delta T cells is similar in infected and uninfected animals. The results clearly indicate that gamma delta T cells in rhesus monkeys are influenced by SIV infection. The detailed analysis of the gamma delta T cell response to SIV infection can serve as a model for understanding human gamma delta T cell responses to HIV infections.

Combined traditional Chinese medicine and Western medicine. Relieving effects of Chinese herbs, ear-acupuncture and epidural morphine on postoperative pain in liver cancer.

In the evaluation of Chinese herbs (A), ear-acupuncture (B) and epidural morphine (C) to relieve postoperative pain and abdominal distension, sixteen male patients with primary liver cancer were observed. This study was conducted by means of orthogonal experiment and double blind, randomized design. The patients received various treatments according to the display of the orthogonal table L16(2)15 which corresponds to 2(3) factorial experiment design. C+ (morphine 2 mg) was given before the peritoneum was sutured. A+ (orally administered) and B+ were given 24 hours after operation. 50-100 mg of pethidine was given when the pain intensity VAS (0-100) exceeded 50-70. The observation parameters included plasma leucine enkephalin (LEK), postoperative total dosage of narcotics administered for 5 days, VAS for pain and pain reliever, abdominal distension, urinary retention, constipation, etc. The results were as follows: a. Patients who had received A (A+B+C+, A+B+C-, A+B-C-, A+B-C+); C (C+A+B+, C+A+B-, C+A-B+, C+A-B-), or B (B+A+C+, B+A+C-, B+A-C+, B+A-C-) produced better analgesic effects than those who had received placebo. The A, B, and C reduced narcotics 650, 450 and 550 mg respectively when compared with placebo. The effects of A and C were of statistical significance (P < 0.05), while AB, BC, and AC interactions were not found; b. A and B minimized abdominal distension and urinary retention, while C prolonged them. As compared with the placebo, A and B accelerated restoration of bowel peristalsis (P < 0.05, ANOVA). Both A and B decreased it for 165 hours, while epidural morphine prolonged it for 49 hours; and c.(ABSTRACT TRUNCATED AT 250 WORDS)