Identification of mega-environments and rice genotypes for general and specific adaptation to saline and alkaline stresses in India.

In the present study, a total of 53 promising salt-tolerant genotypes were tested across 18 salt-affected diverse locations for three years. An attempt was made to identify ideal test locations and mega-environments using GGE biplot analysis. The CSSRI sodic environment was the most discriminating location in individual years as well as over the years and could be used to screen out unstable and salt-sensitive genotypes. Genotypes CSR36, CSR-2K-219, and CSR-2K-262 were found ideal across years. Overall, Genotypes CSR-2K-219, CSR-2K-262, and CSR-2K-242 were found superior and stable among all genotypes with higher mean yields. Different sets of genotypes emerged as winners in saline soils but not in sodic soils; however, Genotype CSR-2K-262 was the only genotype that was best under both saline and alkaline environments over the years. The lack of repeatable associations among locations and repeatable mega-environment groupings indicated the complexity of soil salinity. Hence, a multi-location and multi-year evaluation is indispensable for evaluating the test sites as well as identifying genotypes with consistently specific and wider adaptation to particular agro-climatic zones. The genotypes identified in the present study could be used for commercial cultivation across edaphically challenged areas for sustainable production.

The association of cigarette smoking with alveolar bone loss in postmenopausal females.

BACKGROUND, AIMS: The purpose of this 2-year longitudinal clinical study was to determine the impact of smoking on alveolar bone height and density changes in postmenopausal females. METHODS: 59 postmenopausal women completed this study, including 38 non-smokers and 21 smokers. All subjects had a history of periodontitis, participated in 3- to 4-month periodontal maintenance programs and were within 5 years of menopause at the study outset. 4 vertical bite-wing radiographs of posterior sextants were taken at baseline and 2-year visits. Radiographs were evaluated using computer-assisted densitometric image analysis (CADIA); changes in interproximal alveolar bone density and changes in alveolar bone height were determined. Relative clinical attachment levels (RCAL) and presence/absence of plaque and bleeding on probing were recorded. RESULTS: Smokers exhibited a higher frequency of alveolar bone height loss (p<0.05) and crestal (p<0.03) and subcrestal (p<0.02) density loss relative to non-smokers. Smokers exhibited a trend (p<0.08) toward a higher frequency of > or =2.0 mm RCAL loss over the 2-year period. Plaque and bleeding on probing did not differ between smokers and non-smokers. A significant interaction, determined by repeated measures ANOVA, was noted between systemic bone mineral density (BMD) at the lumbar spine and smoking on alveolar bone density change (p<0.05). Only non-smoking patients with normal BMD realized a mean net gain in alveolar bone density; osteoporotic/osteopenic subjects (n=25) and smokers lost alveolar bone density. CONCLUSION: Postmenopausal female smokers were more likely to lose alveolar bone height and density than non-smokers with a similar periodontitis, plaque and gingival bleeding experience. In addition, both smoking and osteoporosis/osteopenia provided a negative influence on alveolar bone.

Longitudinal alveolar bone loss in postmenopausal osteoporotic/osteopenic women.

The purpose of this 2-year longitudinal clinical study was to investigate alveolar (oral) bone height and density changes in osteoporotic/osteopenic women compared with women with normal lumbar spine bone mineral density (BMD). Thirty-eight postmenopausal women completed this study; 21 women had normal BMD of the lumbar spine, while 17 women had osteoporosis or osteopenia of the lumbar spine at baseline. All subjects had a history of periodontitis and participated in 3- to 4-month periodontal maintenance programs. No subjects were current smokers. All patients were within 5 years of menopause at the start of the study. Four vertical bitewing radiographs of posterior sextants were taken at baseline and 2-year visits. Radiographs were examined using computer-assisted densitometric image analysis (CADIA) for changes in bone density at the crestal and subcrestal regions of interproximal bone. Changes in alveolar bone height were also measured. Radiographic data were analyzed by the t-test for two independent samples. Osteoporotic/osteopenic women exhibited a higher frequency of alveolar bone height loss (p<0.05) and crestal (p<0.025) and subcrestal (p<0.03) density loss relative to women with normal BMD. Estrogen deficiency was associated with increased frequency of alveolar bone crestal density loss in the osteoporotic/osteopenic women and in the overall study population (p<0.05). These data suggest that osteoporosis/osteopenia and estrogen deficiency are risk factors for alveolar bone density loss in postmenopausal women with a history of periodontitis.

Influence of estrogen and osteopenia/osteoporosis on clinical periodontitis in postmenopausal women.

BACKGROUND: In Western societies, more than one-third of the female population above age 65 suffers from signs and symptoms of osteoporosis, a disorder characterized by low bone mass. Estrogen deficiency is the dominant pathogenic factor for osteoporosis in women. The impact of estrogen deficiency and osteopenia/osteoporosis on periodontitis is unclear, partially due to the lack of longitudinal studies evaluating clinical signs of gingival inflammation and periodontitis progression. The purpose of this investigation was to analyze prospectively the influence of serum estradiol levels and osteopenia/osteoporosis on common clinical measurements of periodontal disease over a 2-year period. METHODS: Fifty-nine moderate/advanced adult periodontitis patients and 16 non-periodontitis subjects, all within 5 years after menopause at baseline, completed the study. Serum estradiol levels (E2) were measured yearly by 125I radioimmunoassay, and osteopenia/osteoporosis was determined by dual energy x-ray absorptiometry of the lumbar spine. Posterior interproximal clinical measurements were obtained every 6 months for the periodontitis patients, including explorer-detectable supragingival plaque, bleeding on probing (BOP) and relative clinical attachment level (RCAL). Baseline probing depths, smoking history, and demographic data also were collected. RESULTS: Data indicated that baseline demographic measurements and bone mineral density (BMD) of the lumbar spine were not different between E2-deficient and E2-sufficient subjects. Smoking activity (packs smoked/day, years smoked) was higher in periodontitis patients (P=0.0001). E2-sufficient periodontitis subjects had a higher frequency of supragingival plaque without increasing gingival inflammation. E2 status did not influence the percentage of sites losing RCAL for either periodontitis or non-periodontitis groups, but when non-smoking osteopenic/osteoporotic periodontitis patients were evaluated, E2-deficient subjects had more BOP (43.8% versus 24.4%, P<0.04) and a trend toward a higher frequency of > or =2.0 mm RCAL loss (3.8% versus 1.2%, P<0.1) than E2-sufficient subjects. CONCLUSIONS: These data suggest that E2 supplementation (serum E2>40 pg/ml) is associated with reduced gingival inflammation and a reduced frequency of clinical attachment loss in osteopenic/osteoporotic women in early menopause.

The smoking cessation efficacy of varying doses of nicotine patch delivery systems 4 to 5 years post-quit day.

BACKGROUND: This study was undertaken to evaluate the long-term smoking cessation efficacy of varying doses of transdermal nicotine delivery systems 4 to 5 years post-quit day. METHODS: A follow-up study was conducted 48 to 62 months after quit day among patients who were enrolled in the Transdermal Nicotine Study Group investigation. The latter study included group smoking cessation counseling and randomized assignment to 21, 14, or 7 mg nicotine patches or placebo patches. Seven of nine smoking cessation research centers participated in the long term follow-up investigation. RESULTS: The self-reported continuous quit rate among patients originally assigned 21 mg (20.2%) was significantly higher than rates for patients assigned 14 mg (10.4%), 7 mg (11.8%), or placebo patches (7.4%). Log rank survival analysis found no difference in relapse rates after 1 year postcessation. Smokers under age 30 years were significantly less likely to be abstinent at long term follow-up compared to smokers > or = 30 years of age (3 vs 13%, respectively). Mean weight gain in confirmed continuous quitters was 10.1 kg in men and 8.0 kg in women. Of the 63 continuous abstainers surveyed, 30 respondents (48%) reported that they no longer craved cigarettes, and no individual reported daily craving for cigarettes. CONCLUSIONS: Nicotine patch therapy with 21 mg/day patches resulted in a significantly higher long-term continuous abstinence rate compared to lower dose patches and placebo. Relapse rates among the various treatment conditions were similar after 1 year postcessation.

Nicotine and smokeless tobacco effects on gingival and peripheral blood mononuclear cells.

The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) secretion by peripheral blood mononuclear cells (PBMC, consisting of monocytes and lymphocytes) and gingival mononuclear cells (GMC). Both peripheral blood and gingival tissue adjacent to the alveolar crest were taken from non-smoking adult periodontitis patients. Gingival tissue was treated with collagenase and deoxyribonuclease and GMC and PBMC were isolated by Ficoll-Hypaque centrifugation. GMC and PBMC (100,000 cells/200 microl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1% ST, 100 microg/ml nicotine, 1 microg/ml Porphyromonas gingivalis LPS, or 1 microg/ml P. gingivalis LPS and either 100 microg/ml nicotine or 1% ST. Enzyme immunoassays were used to quantify PGE2 and IL-1beta. Treatments were compared by repeated measures ANOVA. 100 microg/ml nicotine (7-fold, p<0.02) and 1% ST (3.5-fold, p<0.004) significantly increased secretion of PGE2 by PBMC relative to control cultures. 100 microg/ml nicotine and 1% ST, however, had no effect on IL-1beta secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+ 100 microg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 microg/ml nicotine significantly downregulated IL-1beta secretion by GMC relative to medium alone (p<0.008) and had no effect on PGE2 secretion by GMC. These data indicate that while nicotine and ST can stimulate PBMC to secrete PGE2, they cannot activate further mononuclear cells extracted from gingiva, possibly due to maximal previous stimulation in the periodontitis lesion.

Histology near periodontitis osteoclasts.

Histologic evaluation of periodontal tissues generally has included only areas adjacent to the gingival crevice, without knowledge or quantitation of alveolar crest osteoclastic (periodontitis) activity and infiltrate. The purpose of this study was to use human autopsy material to quantitate collagen and cell types adjacent to presumed periodontitis activity and quiescence, each in the same individual. Thirteen subjects contributed 4 sites each, 2 exhibiting alveolar crest periosteal osteoclasts in resorption lacunae/periodontitis activity (OC/PA) and 2 with no osteoclasts or resorption lacunae/ periodontal quiescence (NOC/PQ). Tissue and cell morphotypes were quantitated by 2 evaluators at 100 intersects in 0.06 mm2 fields progressing from the alveolar crest toward the gingival crevice. Cell morphotypes/tissue components were compared between groups and fields using a general linear model with repeated measures. OC/PA fields adjacent to the alveolar crest contained significantly more intersects with macrophage-like cells (10.7+/-1.1 versus 5.3+/-0.6%, P=0.0003), lymphocytes (4.6+/-1.1 versus 0.7+/-0.2%, P=0.0013), plasma cells (13.3+/-2.7 versus 2.1+/-0.6%, P=0.0004), and less with collagen (48.9+/-3.5 versus 75.0+/-2.0%, P=0.0001) than NOC/PQ fields. Numbers of lymphocytes and plasma cells increased (P=0.0006 and P=0.0002, respectively), and fibroblasts and collagen decreased (P=0.0024 and P=0.0001, respectively) in fields up to 1 mm closer to the gingival crevice. However, apparent osteoclastic activity in periodontitis subjects is associated with a significant inflammatory cell infiltrate, especially macrophages and plasma cells.

HLA-D types and serum IgG responses to Capnocytophaga in diabetes and periodontitis.

Serum IgG responses to the cell envelope proteins (CEPs) from Capnocytophaga sputigena, Capnocytophaga ochracea, and Capnocytophaga gingivalis were examined in periodontally healthy and periodontitis subjects, both with and without type 1 diabetes (n = 60). Serum IgG responses to CEPs were determined by immunoblotting with biotin-goat anti-human IgG and an alkaline phosphatase-streptavidin system. Reactivity was analyzed by transmission densitometry, digitization, and computer manipulation. The patients with diabetes showed significantly (p < 0.01) fewer responses to 14 CEPs (from 81 to 10 kDa) from C. sputigena, 5 CEPs (from 90 to 17 kDa) from C. gingivalis, and the 27-kDa CEP from C. ochracea than in the non-diabetic group. The periodontitis patients showed significantly (p < 0.01) fewer responses to the 25- and 11-kDa CEPs from C. sputigena, the 125- and 17-kDa CEPs from C. gingivalis, and the 42-kDa CEP from C. ochracea than in the periodontally healthy group. HLA-DR4, HLA-DR53, and HLA-DQw3 were associated with periodontitis, while only HLA-DR4 was associated with diabetes (p < 0.02). Significant (p < 0.01) correlations were found between HLA-DR2 and IgG reactivity patterns associated with non-diabetics, and between HLA-DR4 and IgG reactivity patterns associated with diabetic and periodontitis subjects. These results indicate that both type 1 diabetics and periodontitis subjects have a depressed IgG antibody profile to Capnocytophaga, which may account for an increased susceptibility to periodontitis infection. Periodontitis in type 1 diabetes may be related more to the HLA-D type and altered immune function than to the diabetes itself.

Experimental gingivitis in periodontitis-susceptible subjects.

The purpose of this study was to evaluate clinical, microbiological, and gingival crevicular fluid (GCF) profiles in periodontitis-resistant and periodontitis-susceptible subjects during 4 weeks of experimental gingivitis. Experimental groups of similar ages were defined as gingivitis controls (GC; n = 10) and history of rapidly progressive periodontitis (RPP; n = 10), respectively. Prior to baseline, all subjects achieved good plaque control (plaque index (P1I) approximately 0) and gingival health (gingival index (GI) = 0), and had probing depths < or = 4 mm on experimental teeth. For 4 weeks after baseline, oral hygiene around maxillary 2nd premolar and 1st molar teeth was inhibited by a plaque guard. The plaque guard was removed weekly for GCF sampling to determine interleukin (IL)-1 beta and prostaglandin (PG)E2 amounts by ELISAs. In addition, P1I, GI, probing depth, and gingival recession measurements were made. Subgingival plaque darkfield microscopy and DNA probe analysis also were performed. Results indicated that clinical signs of inflammation, microbiological patterns and GCF profiles progressed similarly in both groups. However, plaque accumulated more rapidly in the susceptible subjects. P1I in RPP at 4 weeks was 2.1 +/- 0.1 compared to 1.5 +/- 0.2 in GC, with an incidence of P1I > of 100% versus 50%, respectively (logistic regression; p < 0.0001). Hence, the clinical, microbiological and host factors selected for this study were unrelated to previous susceptibility to periodontitis when evaluated in the experimental gingivitis model. However, the increased rate of plaque accumulation, following thorough plaque removal, in RPP patients suggests a potential factor in disease recurrence in these susceptible subjects.

Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators.

Cancer is a disease that begins with mutation of critical genes: oncogenes and tumor suppressor genes. Our research on carcinogenic aromatic hydrocarbons indicates that depurinating hydrocarbon-DNA adducts generate oncogenic mutations found in mouse skin papillomas (Proc. Natl. Acad. Sci. USA 92:10422, 1995). These mutations arise by mis-replication of unrepaired apurinic sites derived from the loss of depurinating adducts. This relationship led us to postulate that oxidation of the carcinogenic 4-hydroxy catechol estrogens (CE) of estrone (E1) and estradiol (E2) to catechol estrogen-3,4-quinones (CE-3, 4-Q) results in electrophilic intermediates that covalently bind to DNA to form depurinating adducts. The resultant apurinic sites in critical genes can generate mutations that may initiate various human cancers. The noncarcinogenic 2-hydroxy CE are oxidized to CE-2,3-Q and form only stable DNA adducts. As reported here, the CE-3,4-Q were bound to DNA in vitro to form the depurinating adduct 4-OHE1(E2)-1(alpha,beta)-N7Gua at 59-213 micromol/mol DNA-phosphate whereas the level of stable adducts was 0.1 micromol/mol DNA-phosphate. In female Sprague-Dawley rats treated by intramammillary injection of E2-3,4-Q (200 nmol) at four mammary glands, the mammary tissue contained 2.3 micromol 4-OHE2-1(alpha, beta)-N7Gua/molDNA-phosphate. When 4-OHE1(E2) were activated by horseradish peroxidase, lactoperoxidase, or cytochrome P450, 87-440 micromol of 4-OHE1(E2)-1(alpha, beta)-N7Gua was formed. After treatment with 4-OHE2, rat mammary tissue contained 1.4 micromol of adduct/mol DNA-phosphate. In each case, the level of stable adducts was negligible. These results, complemented by other data, strongly support the hypothesis that CE-3,4-Q are endogenous tumor initiators.

Self-recognition of alcohol and cigarette dependency among high school seniors.

A brief, anonymous survey of 284 high school seniors at one midwestern metropolitan public high school assessed current smoking, history of alcohol use, and students' beliefs in future risk of dependency. A major purpose was to assess students' self-recognition of alcohol and cigarette dependency. Of the seniors surveyed, 92 (32%) were current smokers, and 237 (84%) reported a previous history of alcohol use. 52% of current smokers indicated they were already "hooked" on cigarettes or anticipated a good chance of cigarette addiction five years later. In contrast, 94% of regular alcohol users indicated there was either no chance (71%) or only a mild chance (23%) of ever becoming an alcoholic. Six of every ten high school smokers surveyed reported that quitting cigarettes for three days would be difficult.

Levels of cigarette consumption and response to periodontal therapy.

Seventy-four patients with moderate to advanced periodontitis were classified by cigarette consumption at the initial exam: heavy smokers (HS) > or = 20 cigarettes/day (n = 31); light smokers (LS) < or = 19 cigarettes/day (n = 15); past smokers (PS) had a history of smoking but had quit by the initial exam (n = 10); and non-smokers (NS) had never smoked (n = 18). All patients were treated with four modalities of periodontal therapy followed by supportive periodontal treatment (SPT) for a period of up to 7 years. Clinical parameters including probing depth (PD), clinical attachment level (CAL), recession (REC), presence of bleeding on probing (BOP), and supragingival plaque (PL) were assessed at six sites around each tooth. Horizontal probing attachment level (HAL) was obtained at molar furcation sites. Data were collected initially, 4 weeks after non-surgical therapy, 10 weeks after surgical therapy, and yearly during SPT. HS and LS demonstrated less PD reduction and less CAL gain than PS and NS following active treatment and throughout SPT. Following active treatment, HAL changes were similar for all groups, but during 7 years of SPT, HS and LS experienced greater loss of HAL. There were no differences in BOP among the four groups. HS demonstrated a higher percentage of PL positive sites compared to the other groups. In summary, HS and LS responded less favorably to therapy than PS and NS. A past history of smoking was not deleterious to the response to therapy.

Long-term evaluation of periodontal therapy: II. Incidence of sites breaking down.

Eighty-two patients were treated in a split mouth design with coronal scaling (CS), root planing (RP), modified Widman surgery (MW), and flap with osseous surgery (FO) which were randomly assigned to the various quadrants in the dentition. Following phase I and phase II therapy, the patients received supportive periodontal treatment (SPT) at 3-month intervals for up to 7 years. Clinical attachment level (CAL) was determined initially, post-phase I, post-phase II and prior to each SPT appointment. If a site lost > or = 3 mm of CAL from its baseline, it was classified as a breakdown site. Baselines were the initial exam for sites treated by CS and 10 weeks post-phase II for sites treated by RP, MW, and FO. Data were grouped by probing depth (PD) severity at the initial exam and at post-phase II. The breakdown for CS sites was assessed separately from RP, MW, and FO sites because of different baselines and retreatment protocols. Sites treated by CS had a higher incidence of breakdown than the other therapies through year 1 of SPT. The breakdown incidences/year for RP and MW sites were similar and greater than for FO sites in 1 to 4 mm and 5 to 6 mm PD categories. Breakdown incidence of RP sites was greater than MW sites which was greater than FO sites initially > or = 7 mm. Differences in incidence of breakdown between therapies after recategorizing data by post-phase II PD were the same as above, except no difference was present between RP and MW sites > or = 7 mm. Breakdown incidences were greater in increasing PD severities regardless of when they were categorized. There was no further loss of CAL one year after retreatment in 88% of sites. Patients with higher breakdown incidences tended to be smokers at the initial exam.

Long-term evaluation of periodontal therapy: I. Response to 4 therapeutic modalities.

Eighty-two periodontal patients were treated in a split mouth design with coronal scaling (CS), root planing (RP), modified Widman surgery (MW), and flap with osseous resection surgery (FO) which were randomly assigned to various quadrants in the dentition. Therapy was performed in 3 phases: non-surgical, surgical, and supportive periodontal treatment (SPT) < or = 7 years. Clinical data consisted of probing depth (PD), clinical attachment level (CAL), gingival recession (REC), bleeding on probing (BOP), suppuration (SUP), and supragingival plaque (PL). Because of the necessity to exit many CS treated sites due to breakdown, data for CS were reported only up to 2 years. All therapies produced mean PD reduction with FO > MW > RP > CS following the surgical phase for all probing depth severities. By the end of year 2 there were no differences between the therapies in the 1 to 4 mm sites. There were no differences in PD reduction between MW and RP treated sites by the end of year 3 in the 5 to 6 mm sites and by the end of year 5 in the > or = 7 mm sites. FO produced greater PD reduction in > or = 5 mm sites through year 7 of SPT. Following the surgical phase, FO produced a mean CAL loss and CS and RP produced a slight gain in 1-4 mm sites. RP and MW produced a greater gain of CAL than CS and FO following the surgical phase in 5 to 6 mm sites, but the magnitude of difference decreased during SPT. Similar CAL gains were produced by RP, MW, and FO in sites > or = 7 mm. These gains were greater than that produced by CS and were sustained during SPT. Recession was produced with FO > MW > RP > CS. This relationship was maintained throughout SPT. The prevalences of BOP, SUP, and PL were greatly reduced throughout the study and were comparable between sites treated by RP, MW, and FO while the CS sites had more BOP and SUP.

Multiple organ dysfunction syndrome in bone marrow transplantation.

OBJECTIVE: To define the frequency and outcome of organ dysfunction in bone marrow transplantation (BMT) and to determine if patients with organ dysfunction have lower levels of protein C (PC) and/or antithrombin III (ATIII) than those without organ dysfunction. DESIGN: Inception cohort of patients undergoing BMT, followed for 28 days, until hospital dismissal, or until death. SETTING: Bone marrow transplant department of a university hospital. PATIENTS: A total of 199 consecutive patients admitted for BMT. INTERVENTIONS: Standard supportive care was given to all patients. MAIN OUTCOME MEASURES: Definitions of organ dysfunction were arrived at prior to beginning the study. They include pulmonary, central nervous system (CNS), hepatic, and renal dysfunction. Protein C and ATIII levels were measured prior to beginning the preparative regimen and weekly thereafter. RESULTS: Single organ dysfunction, manifesting as pulmonary, CNS, or hepatic dysfunction, occurred in 93 (48.5%) of the 199 patients and was a strong predictor of multiple organ dysfunction syndrome (MODS) and death. Death occurred in 14 (7.0%) of the patients. Cause of death was precisely identified in only four patients. Low levels of either PC or ATIII were associated with death and pulmonary, CNS, and hepatic dysfunction. Multivariate analysis showed ATIII and PC levels were associated with single organ dysfunction independent of the type of transplant, the type of preparative regimen, and the presence of bacteremia. CONCLUSIONS: Single organ dysfunction during BMT is a marker for a systemic abnormality that has a high likelihood of progressing to MODS, similar to that seen in other critically ill patient populations. MODS is the leading cause of death in series of BMT patients. Low levels of ATIII and PC are markers of and may be involved in the pathogenesis of MODS in BMT.

Functional and phenotypic characterization of human peripheral blood stem cell harvests: a comparative analysis of cells from consecutive collections.

A considerable number of patients with malignancies who are treated with high-dose therapy and hematopoietic stem cell transplantation subsequently relapse. Analyses of peripheral blood stem cell (PBSC) harvests obtained from 49 cancer patients showed that the PBSC harvest contained precursors for antitumor effector cells. Ex vivo manipulation of these harvests to maximize the antitumor effector cell activity may provide a new therapeutic approach to decrease or eliminate any minimal residual disease that remains after high-dose therapy. Characterization of PBSC from consecutive collections determined the collections best suited for ex vivo augmentation of antitumor cytotoxic effector cells. We report the results of a functional and phenotypical characterization of PBSC obtained from six consecutive collections from 18 cancer patients receiving granulocyte-macrophage colony-stimulating factor (GM-CSF) for hematopoietic stem/progenitor cell mobilization. The PBSC were evaluated for their cytotoxicity using the 51Cr-release assay. The frequency and subsets of lymphocytes were determined using flow cytometry with appropriate specific marker antibodies and differential cell counts. The content of hematopoietic progenitor cells in each collection was determined using a colony-forming unit granulocyte-macrophage (CFU-GM) culture assay. The frequency of cytotoxic effector cells including lymphokine-activated killer (LAK) cell precursors and lymphocytes was significantly greater (P < .05) in the early collections, whereas the later collections contained significantly (P < .05) more CFU-GM progenitor cells and fewer cytotoxic effector cells. Thus, our results show that PBSC obtained from advanced cancer patients do contain considerable levels of precursor cells for the generation of LAK cell populations. These results suggest that cells from the earlier collections are best suited for ex vivo manipulation to augment the antitumor effects.

Smokeless tobacco effects on monocyte secretion of PGE2 and IL-1 beta.

The use of smokeless tobacco (ST) products is associated with mucosal lesions, gingival recession, and attachment loss at the site of tobacco placement. Monocytes/macrophages are primary producers of PGE2 and IL-1 beta, inflammatory mediators which are thought to play a role in the destruction of the periodontium. The purpose of this study was to determine the effect of ST alone and in combination with a major stimulator of inflammation, bacterial lipopolysaccharide (LPS), on monocyte secretion of these mediators. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy donors who were non-ST users. PBM were incubated for 24 hours in RPMI 1640 containing various concentrations of ST (0%, 0.005%, 0.01%, 1%) with or without 10 micrograms/ml LPS (Porphyromonas gingivalis LPS or Escherichia coli LPS). Of the ST preparations, only 1% ST resulted in PBM mediator secretion (7.7 +/- 2.0 ng/ml for PGE2 and 1.3 +/- 0.2 ng/ml for IL-1 beta) above that of control (unstimulated) cultures. Furthermore, the combination of 1% ST and LPS resulted in a potentiation of PGE2 release (5-fold for E. coli LPS + 1% ST and 10-fold for P. gingivalis LPS + 1% ST; P < 0.0001, one-way ANOVA) relative to the LPS preparations alone. In contrast, PBM IL-1 beta release decreased more than 2-fold upon E. coli LPS and 1% ST exposure, relative to treatment with E. coli LPS alone (P < 0.0001, one-way ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of smoking on the response to periodontal therapy.

This study evaluated the effect of smoking on the clinical response to non-surgical and surgical periodontal therapy. 74 adult subjects with moderate to advanced periodontitis were treated according to a split-mouth design involving the following treatment modalities: coronal scaling, root planing, modified Widman surgery, and flap with osseous resectional surgery. Clinical parameters assessed included probing depth, probing attachment level, horizontal attachment level in furcation sites, recession, presence of supragingival plaque and bleeding on probing. Data were collected: initially, 4 weeks following phase-I therapy, 10 weeks following phase-II therapy and on a yearly basis during 6 years of maintenance care. Data analysis demonstrated that smokers exhibited significantly less reduction of probing depth and less gain of probing attachment level when compared to non-smokers immediately following active therapy and during each of the 6 years of maintenance (p < 0.05). A greater loss of horizontal attachment level was evident in smokers at each yearly exam during maintenance therapy (p < 0.05). There were no differences between groups in recession changes. In general, these findings were true for the outcomes following all 4 modalities of therapy and were most pronounced in the deepest probing depth category (> or = 7 mm). Statistical analysis showed a tendency for smokers to have slightly more supragingival plaque and bleeding on probing. In summary, smokers responded less favorably than non-smokers to periodontal therapy which included 3-month maintenance follow-up.

Results of liver transplantation in diabetic recipients.

BACKGROUND: The results of orthotopic liver transplantation (OLTx) in patients with diabetes mellitus (DM) are not well defined. METHODS: Between 1985 and 1991, 45 adult patients with pretransplantation DM (5 type I, 40 type II) underwent OLTx at our center as identified by retrospective chart review. We compared this diabetic recipient group to a case-control nondiabetic group matched for age, gender, primary liver disease, weight, and timing of OLTx. A total of 30 variables were collected and analyzed with McNemar's test for categorical data, paired t tests for continuous data, and survival and repeated measures analysis for longitudinal data. RESULTS: No differences between diabetic and nondiabetic recipients were noted in patient or graft survival, the incidence or severity of rejection, blood transfusions, operative complications, readmissions, major infections, or number of hospital days after OLTx. However, the incidence of minor bacterial (p = 0.046) and minor fungal (p = 0.035) infections were higher in the DM group. Serum blood urea nitrogen (p = 0.02) and creatinine (p = 0.03) levels were also higher in patients with diabetes versus control patients during the first year after OLTx. CONCLUSIONS: In carefully selected patients with pretransplantation DM, OLTx can be accomplished with results similar to nondiabetic recipients in spite of a higher incidence of minor infections and renal dysfunction.