Laboratory Evaluation of Single and Periodic Chlorpyrifos Applications for German Cockroach (Orthoptera: Blattellidae) Control

1984 ◽  
Vol 77 (1) ◽  
pp. 4-9
Author(s):  
T. P. Miller ◽  
R. E. Gold
Keyword(s):  
German Cockroach ◽  
Laboratory Evaluation

Laboratory evaluation of boric acid plus porridge oats and iodofenphos gel as toxic baits against the German cockroach, Blattella germanica (L.) (Dictyoptera: Blattellidae)

1982 ◽  
Vol 72 (2) ◽  
pp. 229-237 ◽  
Author(s):  
G. Barson
Keyword(s):  
Drinking Water ◽  
Boric Acid ◽  
Blattella Germanica ◽  
German Cockroach ◽  
Field Strain ◽  
Minimum Amount ◽  
Laboratory Evaluation ◽  
Cockroach Blattella Germanica ◽  
Gel Culture

AbstractAdults of a field strain of Blattella germanica (L.) resistant to dieldrin and bendiocarb were used to evaluate two insecticide bait formulations, 50% boric acid plus 50% porridge oats and 0·25% iodofenphos gel in comparison with gel alone and culture food. All cockroaches from the boric acid plus oats treatment died in less than 20 days, whereas some that fed on iodofenphos gel, culture food or gel blank survived for 30 days. Both insecticides caused females to drop their oothecae prematurely, and fewer eggs from the boric acid plus oats treatments hatched. More cockroaches exposed to boric acid plus oats bait died outside the harbourages than those from the iodofenphos gel treatments. Boric acid plus oats or iodofenphos gel offered together with culture food were eaten throughout the treatments. With iodofenphos gel alone, no bait was eaten after four days, but mortality continued for 21 days. The minimum amount of insecticide bait required to kill all 100 cockroaches was about 1340 mg iodofenphos gel, and 100·0 mg boric acid plus oats. After exposure for 24 h, all cockroaches died within nine days after exposure to boric acid plus oats, whereas with iodofenphos gel some survived after 21 days. Two further applications of gel bait in the iodofenphos experiments on days 13 and 17 failed to increase mortality although some bait was eaten. B. germanica was killed more quickly by both insecticide baits when deprived of drinking water.

Clinical features and outcome of acquired haemophilia A

2010 ◽  
Vol 30 (03) ◽  
pp. 156-161 ◽  
Author(s):  
R. Gheisari ◽  
B. Bomke ◽  
T. Hoffmann ◽  
R. E. Scharf
Keyword(s):  
Respiratory Diseases ◽  
Care Center ◽  
Treatment Algorithm ◽  
Early Death ◽  
Underlying Disease ◽  
Pulmonary Sarcoidosis ◽  
Relative Increase ◽  
Laboratory Evaluation ◽  
Haemophilia A ◽  
Acquired Haemophilia

SummaryWe have performed a monocenter study on 29 consecutive patients with acquired haemophilia A who were referred for diagnosis and treatment to the Düsseldorf Haemophilia Comprehensive Care Center between March 2001 and February 2010. Patients, methods: 18 men (age: 44–86 years) and 11 women (age: 20–83 years). For laboratory evaluation, a standardized staged protocol of aPTT, FVIII : C activity and concentration, mixing studies with patient and normal plasma, and quantification of inhibitor titers (Bethesda assay) was used. Diagnostic work-up included elaborate examinations for any underlying disease. Results: In 18 (62%) of the 29 patients with acquired haemophilia A, an underlying disorder was identified, including 9 patients with respiratory diseases (31%), 7 patients with autoimmune disorders (24%), one with malignancy, and one with postpartum state, while in 11 patients (38%) acquired haemophilia A remained idiopathic. Haemotherapy of bleeding, suppression or elimination of the inhibitor, and induction of immunotolerance to endogenous FVIII:C were performed according to a treatment algorithm. Predefined clinical endpoints were control of bleeding, eradication of the inhibitor, complete or partial remission (CR, PR), relapse, or early death (≤30 days). Of the 29 patients in total, 22 individuals achieved CR (76%), three had PR, one relapsed, and three died within 30 days (one of acute myocardial infarction while on anti-haemorrhagic treatment, one of sepsis while on immunosuppression due to active acquired haemophilia A, one of lung bleeding in association with pre-existing pulmonary sarcoidosis). Conclusion: This monocenter study demonstrates that control of life-threatening bleeding, eradication of the inhibitor, and induction of tolerance to endogenous FVIII have significantly improved the clinical outcome of acquired haemophilia A. Our data also suggest a shift in underlying disorders associated with acquired haemophilia A, whereby, in comparison to published studies, a relative increase in the proportion of patients with respiratory diseases is present.

Laboratory Evaluation and Clinical Characteristics of 2,132 Consecutive Unselected Patients with Venous Thromboembolism – Results of the Spanish Multicentric Study on Thrombophilia (EMET*-Study)

1997 ◽  
Vol 77 (03) ◽  
pp. 444-451 ◽  
Author(s):  
José Mateo ◽  
Artur Oliver ◽  
Montserrat Borrell ◽  
Núria Sala ◽  
Jordi Fontcuberta ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Odds Ratio ◽  
Protein C ◽  
Protein S ◽  
Laboratory Evaluation ◽  
Clinical Factors ◽  
Recurrent Thrombosis ◽  
Heparin Cofactor Ii ◽  
Crude Odds Ratio ◽  
History Of

SummaryPrevious studies on the prevalence of biological abnormalities causing venous thrombosis and the clinical characteristics of thrombotic patients are conflicting. We conducted a prospective study on 2,132 consecutive evaluable patients with venous thromboembolism to determine the prevalence of biological causes. Antithrombin, protein C, protein S, plasminogen and heparin cofactor-II deficiencies, dysfibrinoge-nemia, lupus anticoagulant and antiphospholipid antibodies were investigated. The risk of any of these alterations in patients with familial, recurrent, spontaneous or juvenile venous thrombosis was assessed. The overall prevalence of protein deficiencies was 12.85% (274/2,132) and antiphospholipid antibodies were found in 4.08% (87/2,132). Ten patients (0.47%) had antithrombin deficiency, 68 (3.19%) protein C deficiency, 155 (7.27%) protein S deficiency, 16 (0.75%) plasminogen deficiency, 8 (0.38%) heparin cofactor-II deficiency and 1 had dysfib-rinogenemia. Combined deficiencies were found in 16 cases (0.75%). A protein deficiency was found in 69 of 303 (22.8%) patients with a family history of thrombosis and in 205/1,829 (11.2%) without a history (crude odds ratio 2.34, 95% Cl 1.72-3.17); in 119/665 (17.9%) patients with thrombosis before the age of 45 and in 153/1,425 (10.7%) after the age of 45 (crude odds ratio 1.81, 95% Cl 1.40-2.35); in 103/616 (16.7%) with spontaneous thrombosis and in 171/1,516 (11.3%) with secondary thrombosis (crude odds ratio 1.58, 95% Cl 1.21-2.06); in 68/358 (19.0%) with recurrent thrombosis and in 206/1,774 (11.6%) with a single episode (crude odds ratio 1.78,95% Cl 1.32-2.41). Patients with combined clinical factors had a higher risk of carrying some deficiency. Biological causes of venous thrombosis can be identified in 16.93% of unselected patients. Family history of thrombosis, juvenile, spontaneous and recurrent thrombosis are the main clinical factors which enhance the risk of a deficiency. Laboratory evaluation of thrombotic patients is advisable, especially if some of these clinical factors are present.

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