[Study on the willingness to quit smoking and its influencing factors among current smokers in rural areas in China].

Objective: To study the willingness of current smokers to quit smoking in rural areas and related factors to provide a reference for tobacco control. Methods: The data were collected from the China Chronic Disease and Risk Factor Surveillance in 2018. A multi-stage stratified cluster sampling was used to select 184 509 residents (≥18 years old); among the residents, 10 241 current smokers in rural areas were included in the study. χ2/F test was used to analyze the factors such as willingness to quit smoking and demographic information, tobacco use, cognition of tobacco-related hazard knowledge, the prevalence of chronic diseases, and other factors. Unconditional multifactor logistic regression analysis was used in multivariate analysis. Results: A total of 3 453 (37.46%) considered quitting smoking in the next 12 months. Logistic regression analysis showed that occasional smokers were more willing to quit smoking than daily smokers (OR=0.693, 95%CI: 0.494-0.971), and those who smoked less than 1 pack per day were more willing to quit than those who smoked 1 pack or more per day (OR=0.628,95%CI: 0.511-0.771), those who had quit smoking within 12 months were more willing to quit than those who had not quit within 12 months (OR=0.438, 95%CI: 0.357-0.537), and those with high awareness of tobacco hazards were more willing to quit smoking (OR=1.056, 95%CI: 1.028-1.086). The differences were statistically significant (P<0.05). Conclusions: The willingness of current smokers in rural areas to quit smoking is related to the smoking situation, smoking intensity, previous smoking cession experience, and knowledge of the specific health effects of smoking. It suggests that health education should be strengthened through more efficient health communication methods in rural areas and provide brief smoking cessation interventions to improve rural smokers' willingness to quit smoking.

A fast radio burst source at a complex magnetized site in a barred galaxy.

Fast radio bursts (FRBs) are highly dispersed, millisecond-duration radio bursts1-3. Recent observations of a Galactic FRB4-8 suggest that at least some FRBs originate from magnetars, but the origin of cosmological FRBs is still not settled. Here we report the detection of 1,863 bursts in 82 h over 54 days from the repeating source FRB 20201124A (ref. 9). These observations show irregular short-time variation of the Faraday rotation measure (RM), which scrutinizes the density-weighted line-of-sight magnetic field strength, of individual bursts during the first 36 days, followed by a constant RM. We detected circular polarization in more than half of the burst sample, including one burst reaching a high fractional circular polarization of 75%. Oscillations in fractional linear and circular polarizations, as well as polarization angle as a function of wavelength, were detected. All of these features provide evidence for a complicated, dynamically evolving, magnetized immediate environment within about an astronomical unit (AU; Earth-Sun distance) of the source. Our optical observations of its Milky-Way-sized, metal-rich host galaxy10-12 show a barred spiral, with the FRB source residing in a low-stellar-density interarm region at an intermediate galactocentric distance. This environment is inconsistent with a young magnetar engine formed during an extreme explosion of a massive star that resulted in a long gamma-ray burst or superluminous supernova.

[Changes of serum lipid profiles and the correlation analysis in clinic-pathological features of pancreatic cancer patients].

Objective: To examine the characteristics of blood lipid profile and the correlation with clinic-pathological features of pancreatic cancer patients. Methods: The clinical and pathological data of 265 pancreatic cancer patients who received radical surgical treatment at Department of General Surgery,Qilu Hospital,Shandong University from January 2013 to September 2020 were collected and analyzed retrospectively. Among the 265 pancreatic cancer patients,there were 170 males and 95 females,with age of (61.0±9.6)years(range:28 to 86 years). General information,lipid indicators and clinic-pathological information were collected from electronic medical record system,and follow-up information gained by telephone. According to level of serum lipid in pancreatic cancer patients,265 patients were divided into dyslipidemia group(n=115) and normal lipid group(n=150). Pearson χ2,Student's t tests, variance analysis or univariate Logistic regression was used to analyze the correlation between dyslipidemia and clinico-pathological characteristics of pancreatic cancer,respectively. Kaplan-Meier survival curve was used to assessed the influence of dyslipidemia on prognosis of pancreatic cancer patients. Results: In 265 pancreatic cancer patients,115(43.4%)of them had dyslipidemias,and the most common form was increase of triglyceride(TG)(72.2%). In pancreatic cancer with dyslipidemias group,patients with body mass index ≥25 kg/m2 had higher proportion than normal lipid group(36.1%(26/72) vs. 21.2%(21/99),χ²=4.643,P=0.031); The proportion of carcinoma located at head of pancreas(83.5%(96/115) vs. 40.7%(61/150),χ²=49.412,P<0.01), staging of T1/T2(79.1%(91/115) vs. 60.7%(91/150),χ²=10.316,P<0.01) and lymphatic metastasis(36.5%(42/115) vs. 22.7%(34/150),χ²=6.007,P<0.01) were higher. In patients of pancreatic cancer, dyslipidemias were closely associated with tumor location(OR=10.529,P<0.01)and body mass index(OR=3.671,P=0.008). Serum lipid profile results showed that TG,total cholesterol and high-density lipoprotein(HDL) disorders were associated with tumor location(P<0.05). TG disorder had association with body mass index(P<0.05), and HDL disorder had association with tumor stage(P<0.05). Moreover, the result of survival analysis showed that dyslipidemia was not a factor to impact the prognosis of pancreatic cancer patients underwent surgery(P>0.05). Conclusions: In pancreatic cancer patients,TG disorder was the most common type of dyslipidemia. Dyslipidemia has closely association with clinicopathologic features,including tumor location,body mass index,tumor stage. However,dyslipidemia had little effect on prognosis of pancreatic cancer patients.

No pulsed radio emission during a bursting phase of a Galactic magnetar.

Fast radio bursts (FRBs) are millisecond-duration radio transients of unknown physical origin observed at extragalactic distances1-3. It has long been speculated that magnetars are the engine powering repeating bursts from FRB sources4-13, but no convincing evidence has been collected so far14. Recently, the Galactic magnetar SRG 1935+2154 entered an active phase by emitting intense soft γ-ray bursts15. One FRB-like event with two peaks (FRB 200428) and a luminosity slightly lower than the faintest extragalactic FRBs was detected from the source, in association with a soft γ-ray/hard-X-ray flare18-21. Here we report an eight-hour targeted radio observational campaign comprising four sessions and assisted by multi-wavelength (optical and hard-X-ray) data. During the third session, 29 soft-γ-ray repeater (SGR) bursts were detected in γ-ray energies. Throughout the observing period, we detected no single dispersed pulsed emission coincident with the arrivals of SGR bursts, but unfortunately we were not observing when the FRB was detected. The non-detection places a fluence upper limit that is eight orders of magnitude lower than the fluence of FRB 200428. Our results suggest that FRB-SGR burst associations are rare. FRBs may be highly relativistic and geometrically beamed, or FRB-like events associated with SGR bursts may have narrow spectra and characteristic frequencies outside the observed band. It is also possible that the physical conditions required to achieve coherent radiation in SGR bursts are difficult to satisfy, and that only under extreme conditions could an FRB be associated with an SGR burst.

The influence of oncolytic reovirus on the biological activities of umbilical cord-derived mesenchymal stem cells.

OBJECTIVE: To investigate the influence of oncolytic reovirus on the biological activities of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) as a novel virotherapy strategy. MATERIALS AND METHODS: The Cell Counting Kit-8 assay was used to detect the viability of hUC-MSCs infected with different multiplicities of infection (MOIs) of reoviruses. The biological activities (proliferation, marker expression, multipotency, and migration) of hUC-MSCs were verified by assaying osteogenic and adipogenic differentiation potential, flow cytometry, and electrical cell-substrate impedance sensing, respectively. RESULTS: The viability of hUC-MSCs slightly decreased by infection with low titers of reoviruses. A MOI of 1 had no effect on the viability of hUC-MSCs within 96 h. The biological activities (proliferation, marker expression, multipotency, and migration) of hUC-MSCs were not affected by reovirus infection at a MOI of 1. CONCLUSIONS: Reovirus at a MOI of 1 had no effect on the biological activities of hUC-MSCs.

FBW7 inhibits nucleus pulposus cells proliferation by downregulation of cyclin E in the intervertebral disc degeneration.

OBJECTIVE: TF-box and WD repeat domain-containing 7 (FBW7), a component of SCF ubiquitin ligase complex, usually acts as a tumor suppressor because it has an ability in the inhibition of cell proliferation. Nevertheless, the role of FBW7 in intervertebral disc degeneration (IDD) is not quite understood. MATERIALS AND METHODS: The total protein and RNA were isolated from patients' disc tissues. WB was carried out to analyze the collagen II and FBW7 protein levels of different Pfirrmann grades disc degeneration. Reverse transcription-polymerase chain reaction (RT-PCR) was used to test the collagen II and FBW7 mRNA expression in these disc samples. NP cells were transfected with siRNA-FWB7 to downregulate the FBW7 expression. SiRNA-NC was used as the sham group. Cyclin E, E2F1, and E2F2 were analyzed with WB and RT-PCR. RESULTS: In this study, different kinds of degenerated disc tissues were analyzed, and it was found that FBW7 was overexpressed in much severe degeneration condition, which was also proved by the IL-1ß stimuli nucleus pulposus (NP) cells degeneration model in vitro. Interestingly, the results showed that FBW7 suppression could reverse the degeneration of NP cells. Furthermore, we found that FBW7 induced NP cell cycle arrest in the G1 phase of and inhibited cell proliferation by upregulating p27 expression in vitro. The overexpression of p27 resulted in the inhibition of cyclin E, which promotes cell proliferation. CONCLUSIONS: Taken together, our study uncovered that FBW7 played an essential inhibitory role in NP cells proliferation, providing new insights that FBW7 may be a potential strategy for IDD treatments.

[Understanding of the lower mediastinal lymph node dissection in the adenocarcinoma of the esophagogastric junction through abdomino-transhiatal approach].

In recent years, the incidence of adenocarcinoma of esophagogastric junction (AEG) keeps increasing. Siewert type II and type III AEG invades at 2-4 cm in the lower esophagus, and it has a higher rate of lower mediastinal lymph node metastasis. Lower mediastinal lymph node clearing through the abdomino-transhiatal (TH) approach is preferred, which can be accomplished by entering the lower mediastinum through the hiatus and mobilize the esophagus upward and the surrounding lymph and connective tissue for approximately 6.5 cm. Using the infracardiac bursa (IBC) as an anatomical landmark improves the safety and operability of the thorough dissection of the lower mediastinum. Total resection of the mesenterium at the esophagogastric junction can entirely dissect the lower mediastinal lymph nodes, which conforms to the safety principles in oncology.

[Association between 24 h urinary sodium excretion and microalbuminuria among Chinese people aged from 18 to 69 years old].

Objective: To analyze the association between 24 h urinary sodium excretion and microalbuminuria (MAU) among Chinese people aged from 18 to 69 years old. Methods: 2 400 subjects aged from 18 to 69 years old were selected form Gaomi and Fushan sites of Shandong Province and Xinyi and Ganyu sites of Jiangsu Province in 2013 by using multi-stage stratified cluster random sampling method. Questionnaire survey, physical measurement and 24 h urine collection were conducted. 2 262 subjects were finally included in the analysis. According to the quartile of 24 h urinary sodium, all subjects were divided into Q1-Q4 groups and the levels of urinary microalbumin and MAU among different groups were compared. The relationship between urinary sodium and MAU was analyzed by multivariate logistic regression analysis. Results: The age of subjects was (42.1±13.5) years old, including 1 124 males (49.7%). The 24 h urine volume, urinary sodium, urine albumin M (P(25), P(75)) and MAU detection rate were (1 411±495) ml, (166.4±71.6) mmol/d, 12.5 (9.6, 17.4) mg/d and 9.0% (203 cases), respectively. With the increase of urinary sodium level, the level of urinary albumin increased (P(trend)<0.001), and the prevalence of MAU also showed an upward trend (P(trend)<0.001). Multivariate logistic regression analysis showed that after adjusting for age, gender, smoking, alcohol consumption, BMI, hypertension and diabetes, the risk of MAU in Q4 group increased by 174% compared with Q1 group, and OR (95%CI) value was 2.74 (1.80-4.16). Conclusion: 24 h urinary sodium is associated with the prevalence of MAU and salt reduction can help reduce MAU.

Dunye Guanxinning Improves Acute Myocardial Ischemia-Reperfusion Injury by Inhibiting Neutrophil Infiltration and Caspase-1 Activity.

Acute myocardial infarction is the most serious manifestation of cardiovascular disease, and it is a life-threatening condition. Dunye Guanxinning (DG) is a protective traditional Chinese patent herbal medicine with high clinical efficacy and suitable for the treatment of myocardial infarction. However, the mechanism through which it is beneficial is unclear. In this study, we hypothesized that DG improves acute myocardial ischemia-reperfusion injury by inhibiting neutrophil infiltration and caspase-1 activity. We found that DG administration decreased infarct size and cardiomyocyte apoptosis and improved left ventricular ejection fraction, fractional shortening, end-systolic volume index, end-systolic diameter, and carotid arterial blood flow output in rats. DG administration also improved hemorheological parameters, myocardial damage biomarkers, and oxidative stress indexes. The findings showed that DG administration inhibited neutrophil infiltration and reduced the serum interleukin-1 beta (IL-1ß) level and myocardial IL-1ß maturation. Moreover, DG administration inhibited caspase-1 activity and activated adenosine monophosphate-activated protein kinase (AMPK) phosphorylation in rat hearts. These results suggested that DG administration inhibits inflammasome activity and IL-1ß release through the AMPK pathway. Our findings support the clinical efficacy of DG and partially reveal its mechanism, which is beneficial for understanding the therapeutic effects of this protective traditional Chinese patent drug.

[Effect of lifestyle intervention among high risk group of chronic diseases in Shenzhen Futian district].

Objective: To evaluate the effect of lifestyle intervention among high risk group of chronic diseases in Shenzhen Futian district. Methods: 12 out of 115 communities were randomly selected in Futian district of Shenzhen city from October to November, 2013, and 1 923 cases were screened by multiple ways as high risk groups of chronic diseases. High risk groups of chronic diseases were divided into intervention group (1 338 cases, from five residential communities and three villages within city) and control group (585 cases, from four residential communities). The intervention group received group based health education activities as well as lifestyle intervention. The intervention group was provided with health management which was mainly lifestyle intervention. No intervention was implemented in the control group. All participants were followed up over two years. 1 563 participants (1 002 in intervention group and 561 in control group) were followed up from October to November, 2015. The changes of lifestyle related outcome indicators were analyzed to examine the effect of intervention. Results: In the intervention group, 21.8% (219 persons) in high risk groups of chronic diseases became healthy individuals and 15.2% (152 persons) became patients with chronic diseases. In the control group, 9.6% (54 persons) in high risk groups of chronic diseases became healthy individuals and 20.5% (115 persons) became patients with chronic diseases. The outcome of the intervention group was better than that of the control group and the difference was statistically significant (χ2=-5.67, P<0.001). The proportion of people who knew how to correctly use of oil control pot in the intervention group increased from 61.00% (61/100) to 80.00% (280/350). The proportion of people who took oil control measures in the intervention group increased from 36.43% (365/1 002) to 56.99%(571/1 002). The changes in the intervention group were statistically different (P<0.001), but there was no statistical difference in the control group over the years (P>0.05). The proportion of people who knew how to correctly use of the salt restriction spoon increased from 81.95% (109/133) to 97.99% (342/349). The proportion of people who took salt control measures increased from 45.61% (457/1 002) to 62.67% (628/1 002) in the intervention group. The changes in the intervention group were statistically different (P<0.001). There was no statistical difference in the control group over the years (P>0.05). Conclusion: The proportion of people who adopted healthy lifestyles has increased after 2 years intervention and the lifestyle intervention demonstrated good effect.

FoxQ1 is a Novel Molecular Target for Pancreatic Cancer and is Associated with Poor Prognosis.

FOXQ1 is an oncogene for a variety of tumors and encodes the forkhead boxrelated transcription factor FoxQ1. However, little is known about the role of FoxQ1 in pancreatic cancer (PC). In this study, we examined FoxQ1 expression in PC cell lines and human PC tissues by quantitative PCR and tissue microarray based immunohistochemical staining (IHC), and investigated the clinical correlation between FoxQ1 tissue levels and the clinicopathological characteristics of PC patients. We found that FoxQ1 mRNA expression was up-regulated both in PC cell lines and tumor tissues. IHC results revealed that FoxQ1 was mainly expressed in the cytoplasm, and to a lesser extent in the nucleus of PC cells. FoxQ1 protein levels were significantly higher in PC tissues when compared with matched non-cancerous tissues, and associated positively with the degree of tumor differentiation. Univariate and multivariate survival analysis revealed that patients with high FoxQ1 expression and advanced TNM stage had poor prognosis (HR=1.856, 95%CI 1.065- 3.234, P=0.029; HR=2.091, 95%CI 1.181-3.705, P=0.01). These data indicate that FoxQ1 expression is negatively associated with the overall survival of PC patients, and that this protein may therefore represent a novel molecular target and new prognostic biomarker for PC.

Meta-analysis demonstrates lack of a relationship between XRCC1-399 gene polymorphisms and susceptibility to hepatocellular carcinoma.

XRCC1-399 allele polymorphisms have been reported to be associated with susceptibility to hepatocellular carcinoma (HCC), but the conclusions of the various studies have been inconsistent. We conducted a meta-analysis of available studies to determine whether XRCC1-399 alleles influence susceptibility to hepatocellular carcinoma. We searched English-language databases, including PubMed, Medline and Embase, using terms such as "hepatocellular carcinoma" (or "HCC"), "X-ray repair cross-complementing group 1" (or "XRCC1") and "genetic polymorphism" (or "SNP"), among others; we also searched Chinese-language databases, including CNKI, VIP, Wanfang Data, and CBM, using terms such as "ganai", "ganxibaoai", "ganzhongliu", "duotaixing", and "X-xian xiufu jiaocha hubu jiyin 1". Eight independent studies, including 1604 HCC cases and 2185 controls, were included. The pooled odds ratio for XRCC1-399 was 0.99 (95% confidence interval = 0.75-1.31). We conclude that XRCC1- 399 gene polymorphisms are unrelated to risk for HCC.

Involvement of NF-κB/miR-448 regulatory feedback loop in chemotherapy-induced epithelial-mesenchymal transition of breast cancer cells.

The epithelial-mesenchymal transition (EMT) induced by chemotherapeutic agents promotes malignant tumor progression; however, the mechanism underlying the drug-induced EMT remains unclear. In this study, we reported that miR-448 is the most downregulated microRNA following chemotherapy. Suppression of miR-448 correlated with EMT induction in breast cancer in vitro and in vivo. With the use of chromatin immunoprecipitation-seq analysis, we demonstrated that miR-448 suppression induces EMT by directly targeting special AT-rich sequence-binding protein-1 (SATB1) mRNA, leading to elevated levels of amphiregulin and thereby, increasing epidermal growth factor receptor (EGFR)-mediated Twist1 expression, as well as nuclear factor κB (NF-κB) activation. On the other hand, we also found that the adriamycin-activated NF-κB directly binds the promoter of miR-448 suppressing its transcription, suggesting a positive feedback loop between NF-κB and miR-448. Furthermore, all patients who received cyclophosphamide (CP), epirubicin plus taxotere/CP, epirubicin plus 5-fluorouracil chemotherapy showed miR-448 suppression, an increased SATB1, Twist1 expression and acquisition of mesenchymal phenotypes. These findings reveal an underlying regulatory pathway, in which the autoregulation between NF-κB and miR-448 is important for restrain miR-448 suppression upon chemotherapy and may have a role in the regulation of chemotherapy-induced EMT. Disruption of the NF-κB-miR-448 feedback loop during clinical treatment may improve the chemotherapy response of human breast cancers in which EMT is a critical component.

Selection of antisense oligonucleotides for reversal of multidrug resistance in breast carcinoma cells.

BACKGROUND: Multidrug resistance (MDR) is a major obstacle in cancer treatment. In the present study, six regions of the mdr1 gene associated with transcription control or translation initiation were selected as targets. Six antisense oligonucleotides (ASODN; AS1-AS6) complementary to the corresponding sequence of the mdr1 gene were synthesized to investigate whether or not blocking the transcription control sites with ASODN could reverse MDR and which ASODN had the best efficiency for reversing MDR in breast carcinoma cells. METHODS: Forty-eight hours after transfection, mdr1 mRNA and P-glycoprotein (Pgp) were determined by RT-PCR, flow cytometry and Rhodamine 123 (Rh123) retention assay. The chemosensitivity of the treated cells was evaluated by MTT assay. RESULTS: A significant reduction in expression of mdr1 mRNA and Pgp was found in four groups (AS1, AS3, AS5 and AS6), accompanying a dysfunction of Pgp. The lowest levels of mdr1 index and Pgp expression were observed in the AS6 group. MTT assay showed that a significant reduction of drug resistance was found in the four groups, especially in the AS6 group, which showed an 8.4-fold reduction in drug resistance for adriamycin and a 10.5-fold reduction in drug resistance for vinblastine. DISCUSSION: These data suggest that the MDR phenotype of breast carcinoma cells could be reversed by ASODN complementary to the transcription control site or translation initiation region. AS6, which is complementary to the translation initiation codon (ATG) of mdr1 cDNA, has the best reversal efficiency.

Interleukin-6 in aseptic loosening of total hip replacement prostheses.

OBJECTIVE: To investigate the level of interleukin-6 (IL-6) expression in the synovial-like interface membrane (SLIM) and in the pseudosynovial tissue surrounding the artificial hip joints, as well as in the pseudosynovial fluid from aseptically loosened total hip replacement (THR) prostheses. METHODS: A series of methods were used in this study including immunohistochemical staining, double immunofluorescence labeling, enzyme-linked immunosorbent assay (ELISA), and reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: IL-6 was found in all SLIM and the pseudosynovial tissue samples from aseptic loosening of THR. Semi-quantitative morphometry showed that IL-6 containing cells were more numerous in the SLIM (911 +/- 197; p < 0.01) and the pseudosynovial tissue samples (883 +/- 310; p < 0.01) than in the control synovial tissue (291 +/- 184). Double labeling confirmed that macrophages and fibroblasts were the predominant cell types expressing IL-6. These findings were confirmed by RT-PCR. ELISA revealed no difference in the IL-6 concentration between the pseudosynovial fluid and the control synovial fluid obtained from the patients undergoing hip arthroscopy. CONCLUSIONS: IL-6 locally produced in SLIM may in a paracrine manner contribute to periprosthetic osteolysis of the nearby bone. In contrast, fluid phase IL-6 does not seem to contribute to this end.

No lymphokines in T-cells around loosened hip prostheses.

Research results have been contradictory about the role of lymphocytes and immune response in aseptic loosening of total hip replacement (THR). Conclusive evidence is still lacking in spite of extensive in vivo and in vitro studies. Our study was designed to check whether T-cells were activated and if they produced lymphokines in synovial membrane-like interface tissue around loosened THRs. Tissue sections were stabilized and permeabilized to allow the cytokine-specific antibodies to penetrate through the cell membrane and the membranes of intracellular organelles. This technique, combined with computer-assisted image analysis, permits the detection and quantitation of lymphokine-producing cells. We found that the number of T-cells was low, and none of the T-cells was activated, as shown by the absence of interleukin-2 receptor (IL-2R) immunoreactivity. There was no cell producing lymphokines, such as interleukin-2 (IL-2), interferon-gamma (IFN-gamma), and tumor necrosis factor-beta (TNF-beta). Our results suggest that T-cell-mediated immune response is not actively involved in aseptic loosening of THR.

Tumor necrosis factor-alpha and its receptors, p55 and p75, in gingiva of adult periodontitis.

Tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine, can stimulate matrix metalloproteinase synthesis and osteoclastic bone resorption. We hypothesized that elevated expression of TNF-alpha and its p55 and p75 receptors (TNF-R) in gingival tissue might associate with periodontitis. Immunohistochemistry was used for the study of the localization of TNF-alpha and its p55 and p75 TNF-R in adult periodontitis (AP) gingival tissue, in comparison with that in healthy control specimens. TNF-alpha and p55 TNF-R were detected in sulcular epithelial basal cells and in monocyte/macrophages, fibroblasts, and endothelial cells in the AP gingival tissue specimens, but mainly in fibroblasts and endothelial cells in control specimens. P75 TNF-R was occasionally found in monocyte/macrophage-like cells in gingival tissue specimens. The percentage of TNF-alpha-containing cells was not increased in AP compared with controls (13.2%+/-6.1% vs. 12.8%+/-7.6%), but, due to the increased cellularity of AP samples, the number of TNF-alpha positive cells/mm2 was clearly increased (1621+/-663 vs. 664+/-191, p > 0.001). Thus, AP gingival tissue has an elevated expression of TNF-alpha and especially its p55 receptor, suggesting that TNF-alpha may contribute to tissue degradation in periodontitis.