The chest X-ray score baseline in predicting continuous oxygen therapy failure in low-risk aged patients after thoracic surgery.

Background: Radiographic severity assessment can be instrumental in diagnosing postoperative pulmonary complications (PPCs) and guiding oxygen therapy. The radiographic assessment of lung edema (RALE) and Brixia scores correlate with disease severity, but research on low-risk elderly patients is lacking. This study aimed to assess the efficacy of two chest X-ray scores in predicting continuous oxygen therapy (COT) treatment failure in patients over 70 years of age after thoracic surgery. Methods: From January 2019 to December 2021, we searched for patients aged 70 years and above who underwent thoracic surgery and received COT treatment, with a focus on those at low risk of respiratory complications. Bedside chest X-rays, RALE, Brixia scores, and patient data were collected. Univariate, multivariate analyses, and 1:2 matching identified risk factors. Receiver operating characteristic (ROC) curves determined score sensitivity, specificity, and predictive values. Results: Among the 242 patients surviving to discharge, 19 (7.9%) patients experienced COT failure. COT failure correlated with esophageal cancer surgeries, thoracotomies (36.8% vs. 9%, P=0.003; 26.3% vs. 9.4%, P=0.004), and longer operation time (3.4 vs. 2.8 h, P=0.003). Surgical approach and RALE score were independent risk factors. The prediction model had an area under the curve (AUC) of 0.839 [95% confidence interval (CI), 0.740-0.938]. Brixia and RALE scores predicted COT failure with AUCs of 0.764 (95% CI, 0.650-0.878) with a cut-off value of 6.027 and 0.710 (95% CI, 0.588-0.832) with a cut-off value of 17.134, respectively, after 1:2 matching. Conclusions: The RALE score predict the risk of COT failure in elderly, low-risk thoracic patients better than the Brixia score. This simple, cheap, and noninvasive method helps evaluate postoperative lung damage, monitor treatment response, and provide early warning for oxygen therapy escalation. Further studies are required to confirm the validity and applicability of this model in different settings and populations.

Association of night-time sleep and day napping with the prevalence of MOSH in young obese men.

BACKGROUND: Obesity in men is also shown to be associated with reduced reproductive potential, and this particular subtype was described as male obesity-associated secondary hypogonadism (MOSH). Recent studies showing the influence of sleep disorders on testosterone levels suggested a potential role of sleep disorders in determining the development of MOSH. OBJECTIVES: To assess the association between night-time sleep duration and day napping and the prevalence of MOSH. MATERIALS AND METHODS: In this cross-sectional study, 226 obese male participants aged 18-30 years were enrolled. Daytime napping and night-time sleep duration data were collected using a standardized self-reported Chinese-language questionnaire. MOSH was defined as obese men (BMI ≥ 30 kg/m2 ) with hypogonadal symptoms and decreased total testosterone level and/or free testosterone level, excluding other causes of hypogonadism. RESULTS: The overall prevalence of MOSH was 48.2% in this study. An inverse association was observed between night sleep duration and the risk of prevalent MOSH. Men who reported fewer than 6 h of night-time sleep had reduced total testosterone and free testosterone levels and an increased risk of MOSH. Further regression analysis revealed that after adjustment for potential confounders, the odds ratio of MOSH for the short night-time sleep group (<6 h vs. 6-8 h) was 6.17 (p = 0.040). No significant association was observed between day napping status and prevalence of MOSH. DISCUSSION AND CONCLUSION: Short night sleep duration was associated with an increased risk of MOSH in the young obese Chinese population. Chronic sleep curtailment has a negative effect on obese men's health in terms of hypogonadism.

Lactate Dehydrogenase B and Pyruvate Oxidation Pathway Associated With Carfilzomib-Related Cardiotoxicity in Multiple Myeloma Patients: Result of a Multi-Omics Integrative Analysis.

Multiple myeloma (MM) is the second most frequent hematologic cancer in the United States. Carfilzomib (CFZ), an irreversible proteasome inhibitor being used to treat relapsed and refractory MM, has been associated with cardiotoxicity, including heart failure. We hypothesized that a multi-omics approach integrating data from different omics would provide insights into the mechanisms of CFZ-related cardiovascular adverse events (CVAEs). Plasma samples were collected from 13 MM patients treated with CFZ (including 7 with CVAEs and 6 with no CVAEs) at the University of Florida Health Cancer Center. These samples were evaluated in global metabolomic profiling, global proteomic profiling, and microRNA (miRNA) profiling. Integrative pathway analysis was performed to identify genes and pathways differentially expressed between patients with and without CVAEs. The proteomics analysis identified the up-regulation of lactate dehydrogenase B (LDHB) [fold change (FC) = 8.2, p = 0.01] in patients who experienced CVAEs. The metabolomics analysis identified lower plasma abundance of pyruvate (FC = 0.16, p = 0.0004) and higher abundance of lactate (FC = 2.4, p = 0.0001) in patients with CVAEs. Differential expression analysis of miRNAs profiling identified mir-146b to be up-regulatein (FC = 14, p = 0.046) in patients with CVAE. Pathway analysis suggested that the pyruvate fermentation to lactate pathway is associated with CFZ-CVAEs. In this pilot multi-omics integrative analysis, we observed the down-regulation of pyruvate and up-regulation of LDHB among patients who experienced CVAEs, suggesting the importance of the pyruvate oxidation pathway associated with mitochondrial dysfunction. Validation and further investigation in a larger independent cohort are warranted to better understand the mechanisms of CFZ-CVAEs.

Prevalence of polycystic ovary syndrome in Chinese obese women of reproductive age with or without metabolic syndrome.

OBJECTIVE: To compare the prevalence of polycystic ovary syndrome (PCOS) and related clinical characteristics between metabolically unhealthy obese (MUO) and metabolically healthy obese (MHO) women of reproductive age. DESIGN: Cross-sectional clinical study. SETTING: Tertiary hospital. PATIENT(S): We studied 299 MUO and 122 MHO Chinese women matched on body mass index. Metabolically healthy obese was defined as obesity with no more than one metabolic abnormality. Diagnosis of PCOS was based on the revised Rotterdam criteria. INTERVENTION(S): Each subject underwent physical examination, laboratory evaluation, and gynecologic ultrasound for a diagnosis of PCOS or metabolic syndrome (MetS). MAIN OUTCOME MEASURE(S): Prevalence of PCOS was calculated in both groups. Insulin resistance was determined by homeostasis model assessment of insulin resistance or by the insulin sensitivity index derived from Bergman's minimal model. Fat distribution was measured with computerized tomography scan. RESULT(S): Prevalence of PCOS and its components did not differ between MUO and BMI-matched MHO groups (67.89% and 66.96%, respectively). In logistic regression analysis, MetS did not predict the presence of PCOS after adjusting for confounding factors. The MHO group had lower visceral adipose tissue, relatively higher insulin sensitivity, and better ß-cell function, compared with those in the MUO group; but there were no significant differences in sex hormones (except for free T and sex hormone-binding globulin) and ultrasound manifestations between MHO and MUO women. CONCLUSION(S): For the first time, our findings suggest that MetS does not add additional risk for PCOS. In addition, we found that both MUO and MHO are associated with insulin resistance to some extent.

Increased IFN-α-producing plasmacytoid dendritic cells (pDCs) in human Th1-mediated type 1 diabetes: pDCs augment Th1 responses through IFN-α production.

Increasing evidence suggests that type 1 IFN (IFN-αß) is associated with pathogenesis of Th1-mediated type 1 diabetes (T1D). A major source of IFN-αß is plasmacytoid dendritic cells (pDCs). In this study, we analyzed peripheral blood pDC numbers and functions in at-risk, new-onset, and established T1D patients and controls. We found that subjects at risk for T1D and new-onset and established T1D subjects possessed significantly increased pDCs but similar number of myeloid DCs when compared with controls. pDC numbers were not affected by age in T1D subjects but declined with increasing age in control subjects. It was demonstrated that IFN-α production by PBMCs stimulated with influenza viruses was significantly higher in T1D subjects than in controls, and IFN-α production was correlated with pDC numbers in PBMCs. Of interest, only T1D-associated Coxsackievirus serotype B4 but not B3 induced majority of T1D PBMCs to produce IFN-α, which was confirmed to be secreted by pDCs. Finally, in vitro studies demonstrated IFN-α produced by pDCs augmented Th1 responses, with significantly greater IFN-γ-producing CD4(+) T cells from T1D subjects. These findings indicate that increased pDCs and their IFN-αß production may be associated with this Th1-mediated autoimmune disease, especially under certain viral infections linked to T1D pathogenesis.

C-Abl inhibitor imatinib enhances insulin production by ß cells: c-Abl negatively regulates insulin production via interfering with the expression of NKx2.2 and GLUT-2.

Chronic myelogenous leukemia patients treated with tyrosine kinase inhibitor, Imatinib, were shown to have increased serum levels of C-peptide. Imatinib specifically inhibits the tyrosine kinase, c-Abl. However, the mechanism of how Imatinib treatment can lead to increased insulin level is unclear. Specifically, there is little investigation into whether Imatinib directly affects ß cells to promote insulin production. In this study, we showed that Imatinib significantly induced insulin expression in both glucose-stimulated and resting ß cells. In line with this finding, c-Abl knockdown by siRNA and overexpression of c-Abl markedly enhanced and inhibited insulin expression in ß cells, respectively. Unexpectedly, high concentrations of glucose significantly induced c-Abl expression, suggesting c-Abl may play a role in balancing insulin production during glucose stimulation. Further studies demonstrated that c-Abl inhibition did not affect the major insulin gene transcription factor, pancreatic and duodenal homeobox-1 (PDX-1) expression. Of interest, inhibition of c-Abl enhanced NKx2.2 and overexpression of c-Abl in ß cells markedly down-regulated NKx2.2, which is a positive regulator for insulin gene expression. Additionally, we found that c-Abl inhibition significantly enhanced the expression of glucose transporter GLUT2 on ß cells. Our study demonstrates a previously unrecognized mechanism that controls insulin expression through c-Abl-regulated NKx2.2 and GLUT2. Therapeutic targeting ß cell c-Abl could be employed in the treatment of diabetes or ß cell tumor, insulinoma.

ACE2 and Ang-(1-7) confer protection against development of diabetic retinopathy.

Despite evidence that hyperactivity of the vasodeleterious axis (ACE/angiotensin II (Ang II)/AT1 receptor) of the renin-angiotensin system (RAS) is associated with the pathogenesis of diabetic retinopathy (DR) use of the inhibitors of this axis has met with limited success in the control of this pathophysiology. We investigated the hypothesis that enhancing the local activity of the recently established protective axis of the RAS, ACE2/Ang-(1-7), using adeno-associated virus (AAV)-mediated gene delivery of ACE2 or Ang-(1-7) would confer protection against diabetes-induced retinopathy. Genes expressing ACE2 and Ang-(1-7) were cloned in AAV vector. The effects of ocular AAV-ACE2/Ang-(1-7) gene transfer on DR in diabetic eNOS(-/-) mice and Sprague-Dawley (SD) rats were examined. Diabetes was associated with approximately tenfold and greater than threefold increases in the ratios of ACE/ACE2 and AT1R/Mas mRNA levels in the retina respectively. Intraocular administration of AAV-ACE2/Ang-(1-7) resulted in significant reduction in diabetes-induced retinal vascular leakage, acellular capillaries, infiltrating inflammatory cells and oxidative damage in both diabetic mice and rats. Our results demonstrate that DR is associated with impaired balance of retinal RAS. Increased expression of ACE2/Ang-(1-7) overcomes this imbalance and confers protection against DR. Thus, strategies enhancing the protective ACE2/Ang-(1-7) axis of RAS in the eye could serve as a novel therapeutic target for DR.

An effective way to biosynthesize α-glucosyl eugenol with a high yield by Xanthomonas maltophilia.

CONTEXT: Eugenol is known for its analgesic, local anesthetic, anti-inflammatory, antibacterial, and hair growing effects, the application of which, however, is limited by its low solubility, liability of sublimating, and its pungent smell. Compared to eugenol, its glycosylated derivate [eugenol α-glucoside (α-EG)] has more advantages in application. OBJECTIVE: The biosynthesis of α-EG by Xanthomonas maltophilia Hugh (Xanthomonadaceae) BT-112 and the optimum conditions for α-EG production are investigated here. MATERIALS AND METHODS: The α-EG was obtained by fermentation using Xanthomonas maltophilia BT-112 and purified by macroporous absorption resin. The identity of α-EG is confirmed by high performance liquid chromatography (HPLC) and nuclear magnetic resonance (NMR). RESULTS: The maximum yield of α-EG reached 10.62 g/L broth when the suspension of Xanthomonas maltophilia strain was incubated at 30°C with 70 mM eugenol and 1.0 M maltose. DISCUSSION AND CONCLUSION: Bio-fermentation was applied in this work to get α-EG with a high mole conversion, which is a potentially efficient and highly promising approach to modify phenolic compounds into glucosides.

Gene transfer of angiotensin-converting enzyme 2 in the nucleus tractus solitarius improves baroreceptor heart rate reflex in spontaneously hypertensive rats.

The renin-angiotensin system (RAS) in the nucleus tractus solitarius (NTS) is an important modulator of the baroreceptor heart rate reflex. This study tested the hypothesis that angiotensin-converting enzyme 2 (ACE2) expression is decreased in the NTS of spontaneously hypertensive rats (SHRs) and that its gene transfer in this nucleus would lead to beneficial effects on baroreflex function since this enzyme is key in the regulation of the vasoprotective axis of the RAS. ACE2 protein levels and its activity were significantly decreased in the NTS of SHRs compared to normotensive Wistar-Kyoto (WKY) control rats. Rats instrumented with radio-telemetry transducers received NTS microinjection of either Lenti-ACE2 (Lentiviral vector-mediated gene transfer of ACE2) or lenti-GFP (green fluorescent protein). The ACE2 gene transfer into the NTS resulted in long-term overexpression of ACE2. This was associated with a 60% increase in heart rate baroreflex sensitivity in the lenti-ACE2 injected SHRs compared with the lenti-GFP injected control SHRs (0.27 ± 0.02 ms/mmHg in lenti-GFP rats vs. 0.44 ± 0.07 ms/mmHg in lenti-ACE2 rats). These observations demonstrate that ACE2 gene transfer overcomes its intrinsic decrease in the NTS of SHRs and improves baroreceptor heart rate reflex.

Prevention of pulmonary hypertension by Angiotensin-converting enzyme 2 gene transfer.

In spite of recent advancements in the treatment of pulmonary hypertension, successful control has yet to be accomplished. The abundant presence of angiotensin-converting enzyme 2 (ACE2) in the lungs and its impressive effect in the prevention of acute lung injury led us to test the hypothesis that pulmonary overexpression of this enzyme could produce beneficial outcomes against pulmonary hypertension. Monocrotaline (MCT) treatment of mice for 8 weeks resulted in significant increases in right ventricular systolic pressure, right ventricle:left ventricle plus septal weight ratio, and muscularization of pulmonary vessels. Administration of a lentiviral vector containing ACE2, 7 days before MCT treatment prevented the increases in right ventricular systolic pressure (control: 25+/-1 mm Hg; MCT: 44+/-5 mm Hg; MCT+ACE2: 26+/-1 mm Hg; n=6; P<0.05) and right ventricle:left ventricle plus septal weight ratio (control: 0.25+/-0.01; MCT: 0.31+/-0.01; MCT+ACE2: 0.26+/-0.01; n=8; P<0.05). A significant attenuation in muscularization of pulmonary vessels induced by MCT was also observed in animals overexpressing ACE2. These beneficial effects were associated with an increase in the angiotensin II type 2 receptor:angiotensin II type 1 receptor mRNA ratio. Also, pulmonary hypertension-induced increases in proinflammatory cytokines were significantly attenuated by lentiviral vector-containing ACE2 treatment. Furthermore, ACE2 gene transfer in mice after 6 weeks of MCT treatment resulted in a significant reversal of right ventricular systolic pressure. These observations demonstrate that ACE2 overexpression prevents and reverses right ventricular systolic pressure and associated pathophysiology in MCT-induced pulmonary hypertension by a mechanism involving a shift from the vasoconstrictive, proliferative, and fibrotic axes to the vasoprotective axis of the renin-angiotensin system and inhibition of proinflammatory cytokines.

Evidence for angiotensin-converting enzyme 2 as a therapeutic target for the prevention of pulmonary hypertension.

RATIONALE: It has been proposed that an activated renin angiotensin system (RAS) causes an imbalance between the vasoconstrictive and vasodilator mechanisms involving the pulmonary circulation leading to the development of pulmonary hypertension (PH). Recent studies have indicated that angiotensin-converting enzyme 2 (ACE2), a member of the vasoprotective axis of the RAS, plays a regulatory role in lung pathophysiology, including pulmonary fibrosis and acute lung disease. Based on these observations, we propose the hypothesis that activation of endogenous ACE2 can shift the balance from the vasoconstrictive, proliferative axis (ACE-Ang II-AT1R) to the vasoprotective axis [ACE2-Ang-(1-7)-Mas] of the RAS, resulting in the prevention of PH. OBJECTIVES: We have taken advantage of a recently discovered synthetic activator of ACE2, XNT (1-[(2-dimethylamino) ethylamino]-4-(hydroxymethyl)-7-[(4-methylphenyl) sulfonyl oxy]-9H-xanthene-9-one), to study its effects on monocrotaline-induced PH in rats to support this hypothesis. METHODS: The cardiopulmonary effects of XNT were evaluated in monocrotaline-induced PH rat model. MEASUREMENTS AND MAIN RESULTS: A single subcutaneous treatment of monocrotaline in rats resulted in elevated right ventricular systolic pressure, right ventricular hypertrophy, increased pulmonary vessel wall thickness, and interstitial fibrosis. These changes were associated with increases in the mRNA levels of renin, ACE, angiotensinogen, AT1 receptors, and proinflammatory cytokines. All these features of PH were prevented in these monocrotaline-treated rats by chronic treatment with XNT. In addition, XNT caused an increase in the antiinflammatory cytokine, IL-10. CONCLUSIONS: These observations provide conceptual support that activation of ACE2 by a small molecule can be a therapeutically relevant approach for treating and controlling PH.

Porphyromonas gingivalis htrA is involved in cellular invasion and in vivo survival.

HtrA is a heat-stress protein that functions both as a chaperone and as a serine protease. HtrA has been shown in several organisms to be involved in responses to stressful environmental conditions and involvement of HtrA in virulence has been reported in pathogenic species. A Porphyromonas gingivalis htrA mutant demonstrated no significant difference to the W83 parent strain when subjected to high temperature and pH values from 3 to 11. However, the htrA mutant showed increased sensitivity to H(2)O(2). Cell invasion assays indicated that the total interaction (adherence) with KB cells, human coronary artery endothelial cells and gingival epithelial cells (GEC) was the same for both the wild-type and the htrA mutant. However, the htrA mutant showed increased invasion in KB cells and GEC. Microarray experiments indicated that a total of 253 genes were differentially regulated in the htrA mutant, including a group of stress-related genes, which might be responsible for the observed decreased resistance to H(2)O(2). In animal experiments, a competition assay showed that the htrA mutant did not survive as well as the wild-type. In another in vivo assay, fewer mice infected with the htrA mutant died than mice infected with W83, suggesting that the htrA gene is virulence-related. These data indicate that the htrA gene in P. gingivalis does not relate to stress conditions such as high temperature and pH, but rather to H(2)O(2) stress. The htrA gene also appears to be important for virulence and survival in in vivo animal models.

Cardiac overexpression of angiotensin converting enzyme 2 protects the heart from ischemia-induced pathophysiology.

Angiotensin converting enzyme 2 (ACE2) has been linked to cardiac dysfunction and hypertension-induced cardiac pathophysiology. In this study, we used a gene overexpression approach to investigate the role of ACE2 in cardiac function and remodeling after myocardial infarction. Rats received an intracardiac injection of 4.5x10(8) lentivirus containing ACE2 cDNA, followed by permanent coronary artery ligation (CAL) of the left anterior descending artery. At 24 hours and 6 weeks after surgery, cardiac functions, viability, and pathophysiology were assessed by MRI) and by histological analysis. At 24 hours post-CAL, left ventricular (LV) anterior wall motion was stunted to the same extent in control CAL and lenti-ACE2-treated CAL rats. However lenti-ACE2-treated CAL rats showed a 60% reduction in delayed contrast-enhanced LV volume after gadodiamide injection, indicating early ischemic protection of myocardium by ACE2. At 6 weeks after CAL, lenti-ACE2 rats demonstrated a complete rescue of cardiac output, a 41% rescue of ejection fraction, a 44% rescue in contractility, a 37% rescue in motion, and a 53% rescue in LV anterior (infracted) wall thinning compared with control CAL rats. No changes were observed in the LV posterior (noninfarcted) wall other than an 81% rescue in motion produced by ACE2 in CAL rats. Finally, infarct size measured by 2,3,5-triphenyl-tetrazolium chloride staining was not significantly different between the ligated groups. These observations demonstrate that cardiac overexpression of ACE2 exerts protective influence on the heart during myocardial infarction by preserving cardiac functions, LV wall motion and contractility, and by attenuating LV wall thinning.

The Porphyromonas gingivalis clpB gene is involved in cellular invasion in vitro and virulence in vivo.

ClpB, a component of stress response in microorganisms, serves as a chaperone, preventing protein aggregation and assisting in the refolding of denatured proteins. A clpB mutant of Porphyromonas gingivalis W83 demonstrated increased sensitivity to heat stress, but not to hydrogen peroxide and extreme pHs. In KB cells, human coronary artery endothelial (HCAE) cells and gingival epithelial cells, the clpB mutant exhibited significantly decreased invasion suggesting that the ClpB protein is involved in cellular invasion. Transmission electron microscopic analysis showed that the clpB mutant was more susceptible to intracellular killing than the wild-type strain in HCAE cells. The global genetic profile of the clpB mutant showed that 136 genes belonging to several different cellular function groups were differentially regulated, suggesting that ClpB is ultimately involved in the expression of multiple P. gingivalis genes. A competition assay in which a mixture of wild-type W83 and the clpB mutant were injected into mice demonstrated that the clpB mutant did not survive as well as the wild type. Additionally, mice treated with the clpB mutant alone survived significantly better than those treated with the wild-type strain. Collectively, these data suggest that ClpB, either directly or indirectly, plays an important role in P. gingivalis virulence.

ACE2 gene transfer attenuates hypertension-linked pathophysiological changes in the SHR.

Recently discovered, angiotensin-converting enzyme-2 (ACE2) is an important therapeutic target in the control of cardiovascular diseases as a result of its proposed central role in the control of angiotensin peptides. Thus our objective in the present study was to determine whether ACE2 gene transfer could decrease high blood pressure (BP) and would improve cardiac dysfunctions induced by hypertension in the spontaneously hypertensive rat (SHR) model. Five-day-old SHR and normotensive WKY rats received a single intracardiac bolus injection of lentiviral vector containing either murine ACE2 (ACE2) or control enhanced green fluorescent protein (EGFP) genes. Systolic BP, cardiac functions, and perivascular fibrosis were evaluated 4 mo after ACE2 gene transduction. ACE2 gene transfer resulted in a significant attenuation of high BP in the SHR (149 +/- 2 mmHg in lenti-ACE2 vs. 180 +/- 9 mmHg in lenti-EGFP, P < 0.01). In contrast, no significant effect of lenti-ACE2 on BP of WKY rats was observed. Lenti-ACE2-treated SHR showed an 18% reduction in left ventricular wall thickness (1.52 +/- 0.04 vs. 1.86 +/- 0.04 mm in lenti-EGFP, P < 0.01). In addition, there was a 12% increase in left ventricular end diastolic and a 21% increase in end systolic diameters in lenti-ACE2-treated SHR. Finally, lenti-ACE2 treatment resulted in a significant attenuation of perivascular fibrosis in the SHR. In contrast, ACE2 gene transfer did not influence any of these parameters in WKY rats. These observations demonstrate that ACE2 overexpression exerts protective effects on high BP and cardiac pathophysiology induced by hypertension in the SHR.

Microarray analysis of quorum-sensing-regulated genes in Porphyromonas gingivalis.

Quorum sensing is a phenomenon defined as gene regulation in response to cell density that regulates various functions in bacteria. The periodontopathogen Porphyromonas gingivalis possesses a luxS gene homologue that may encode a quorum-sensing system. In order to identify genes of P. gingivalis that are regulated by luxS, gene expression analysis was done using microarrays and RNA samples from the W83 wild-type strain and an isogenic luxS mutant, LY2001. The results indicated that 17 open reading frames (ORFs) in LY2001 are upregulated and two are downregulated. Real-time PCR was done to confirm the microarray results. Among the upregulated ORFs is a group of stress-related genes, including htrA, clpB, groEL, dnaK, and the F subunit of alkyl hydroperoxide reductase. This suggested that luxS is involved in stress gene regulation in P. gingivalis. Stress response experiments, including high-temperature survival, resistance to hydrogen peroxide (H2O2), and survival during exposure to low and high pH, were performed on the P. gingivalis wild-type and LY2001 strains. LY2001 had a significantly higher survival rate than did W83 when stressed at 50 degrees C. No difference was found at pH 5, but LY2001 had increased survival compared to W83 at pH 9. LY2001 also survived better than W83 when stressed with 0.35 mM H2O2. These results suggest that luxS might be involved in promoting survival of P. gingivalis in the host by regulating its response to host-induced stresses such as temperature, H2O2, and pH.