Probabilistic estimation of the economic effect of operating accidents in the oil and gas industry.

Performance of the company staff is determined by the proficiency of available personal resources. Some of the respective key indicators could be influenced by planner, but most of them are out of direct control. This opens the strong demand on reliable prediction modeling. Decision maker is interested not only in knowing of labor supply/demand situation, but also about the proficiency and reliability of employees. Presented work is intended to find out, which statistical methods are suitable for certain aspects of the staff planning process. General broad modeling of stochastically changing workforce availability numbers could be considered like a description of the random events observation. These events could be categorized and forecasted by the mean of further development of NPI (nonparametric predictive inference) method suggested by Augustin and Coolen. Its capability to learn from multinomial data, especially such as strongly influenced by business environment, geography, state policy, etc., extracted from market reports, and induced from managerial experience seems to be promising. After demand and supply of workforce is forecasted, manager must start the process of hiring. Individual staff evaluation is also quite challenging because of lack or incorrectness of initial information about possible profile type of the candidate. Dempster-Shafer Theory may be good one, but speaking of "gambles" could disappoint many HRspecialists. So, adaptation of the Theory of Adaptive Utility proposed by Houlding and Coolen is assumed as perspective tool for solving this problem. HR decision maker can also follow this kind of sequential process. When the completion of team and groups is done, the labor activity begins. Here, each employee demonstrates his performance rate, qualification and reliability. In this case interaction between workers is strongly matters. Conditional probability is in charge of that kind of evaluation and therefore Bayesian schemes and Walley technique are further developed and applied. Dismissed employees flowing out of the firm again into workforce market and will be available for other companies, also for competitors. Feedback to initial step is recommended.

Transdermal nicotine therapy and primary care. Importance of counseling, demographic, and participant selection factors on 1-year quit rates. The Nebraska Primary Practice Smoking Cessation Trial Group.

OBJECTIVE: To evaluate the smoking cessation efficacy of nicotine patch therapy as an adjunct to low-intensity, primary care intervention. DESIGN: Randomized, placebo-controlled, double-blind, multisite trial. SETTINGS: Twenty-one primary care sites in Nebraska. PATIENTS: A total of 369 smokers of 20 or more cigarettes per day. INTERVENTION: Two brief primary care visits for smoking intervention with 10 weeks of active or placebo-patch therapy. MAIN OUTCOME MEASURES: Confirmed self-reported abstinence 3, 6, and 12 months after the quit day. RESULTS: Compared with placebo control subjects, participants assigned nicotine patches had higher 3-month (23.4% vs 11.4%; P < .01) and 6-month (18.5% vs 10.3%; P < .05) abstinence rates. The 1-year abstinence rates for the active and placebo patch groups were 14.7% and 8.7%, respectively (P = .07). Of smokers aged 45 years and older, 9 (18.8%) of 48 using active patches compared with 0 of 31 using placebo patches achieved 12-month abstinence (chi 2 = 6.56; P < .05). Among those with high nicotine dependency scores (Fagerstrom score > or = 7), 1-year abstinence rates were significantly higher in the nicotine patch group (19.1%) compared with the placebo group (5.0%) (chi 2 = 10.7; P = .001). However, there was no significant difference in 1-year quit rates for participants with low Fagerstrom scores (< 7). CONCLUSIONS: Nicotine patch therapy enhanced 6 month quit rates as an adjunct to brief primary care intervention. The highest quit rates were achieved by participants who specifically contacted the site to enroll in the study or to obtain a prescription for nicotine patches. Differences in participant selection factors may account, in part, for the lower smoking cessation rates associated with primary care intervention. Duration of counseling, patient age, and Fagerstrom scores may be important factors related to the long-term smoking cessation success of nicotine patch therapy.

Inhibitors of nitric oxide synthase attenuate human neutrophil chemotaxis in vitro.

Products released through the L-arginine/nitric oxide biosynthetic pathway regulate soluble guanyl cyclase activity, which in turn modulates polymorphonuclear leukocyte chemotaxis. We hypothesized that inhibitors of nitric oxide synthase attenuate polymorphonuclear leukocyte chemotaxis in vitro. To test this hypothesis, unstimulated polymorphonuclear leukocytes were pretreated with buffer or the nitric oxide synthase inhibitors NG-monomethyl-L-arginine (L-NMMA), NG-nitro-L-arginine methyl ester, and L-canavanine before being exposed to three structurally unrelated chemoattractants, N-formyl-methionyl-leucyl-phenylalanine, C5a des arginine, and leukotriene B4. Polymorphonuclear leukocyte chemotaxis was quantified with a modified blind-well chamber technique. We found that L-NMMA and L-canavanine but not NG-nitro-L-arginine significantly attenuated polymorphonuclear leukocyte chemotaxis (p < 0.05). L-Arginine but not D-arginine, the nitric oxide donor sodium nitroprusside, and 8-bromo-cyclic guanosine monophosphate restored polymorphonuclear leukocyte chemotaxis attenuated by L-NMMA. Chemotaxis of polymorphonuclear leukocytes primed with lipopolysaccharide (Escherichia coli 0127:B8) or phorbol-13-butyrate was also significantly attenuated by pretreatment with L-NMMA and L-canavanine. Consistent with these observations, intracellular concentrations of cyclic guanosine monophosphate in polymorphonuclear leukocytes was decreased by L-NMMA during exposure to N-formyl-methionyl-leucyl-phenylalanine. These data indicate that nitric oxide synthase inhibitors attenuate chemotaxis of unstimulated and primed polymorphonuclear leukocytes in vitro. We suggest that the L-arginine/nitric oxide biosynthetic pathway plays an important role in regulating polymorphonuclear leukocyte emigration in vivo.

Nitric oxide synthase inhibitors attenuate human monocyte chemotaxis in vitro.

Nitric oxide synthase (NOS) inhibitors have been shown to modulate neutrophil migration. We hypothesized that the NOS inhibitors NG-monomethyl-L-arginine (L-NMMA), NG-nitro-L-arginine methyl ester (L-NAME), and L-canavanine (L-CAN) also modulate human peripheral blood monocyte chemotaxis. To test this hypothesis, monocyte chemotaxis toward formylmethionylleucyl-phenylalanine (fMLP) was assessed using a modified blindwell chemotaxis chamber technique. L-NMMA and L-NAME, but not D-NMMA or L-CAN, significantly attenuated fMLP-induced monocyte chemotaxis (P < .05). L-Arginine and sodium nitroprusside, but not D-arginine, reversed NOS inhibitor-induced responses. Dibutryl cyclic guanyl monophosphate (cGMP) attenuated the inhibitory effects of L-NMMA on monocyte chemotaxis (P < .05). Finally, fMLP increased cGMP generation by monocytes, which was significantly attenuated by L-NMMA (P < .05). These data indicate that the L-arginine/NO biosynthetic pathway regulates human monocyte chemotaxis in vitro.

Bovine bronchial epithelial cells metabolize L-arginine to L-citrulline: possible role of nitric oxide synthase.

The conversion of L-arginine to L-citrulline is catalyzed by nitric oxide synthase (NOS), and results in the release of nitric oxide (NO). We hypothesized that bronchial epithelial cells metabolize L-arginine to L-citrulline. We found that cell lysates obtained from unstimulated, cultured bovine bronchial epithelial cells (BBECs) converted L-[3H]arginine to L-[3H]citrulline. This conversion was attenuated by three competitive NOS inhibitors and modulated by lipopolysaccharide and cigarette smoke extract (p < 0.01, all comparisons). These data demonstrate that BBECs metabolize L-arginine to L-citrulline and implicate a role for the L-arginine:NOS biosynthetic pathway in modulating airway responses.