Langerhans' cell histiocytosis in association with periapical granulomas and cysts.

This report describes a series of six cases of inflammatory periapical disease with small aggregates of Langerhans cells as a minor component. Immunohistochemical findings confirm that the cells are phenotypically related to Langerhans cells. Aggregates of these cells are not normally found in radicular cysts or periapical granulomas and have been interpreted to represent chronic localized Langerhans' cells histiocytosis. Whether these lesions, which arise within the context of chronic inflammatory periapical disease, represent incipient eosinophilic granulomas or are a more benign, minimally destructive form of Langerhans' cell histiocytosis is unknown. Clinical follow-up suggests that these lesions remain localized and that curettage is adequate treatment.     

雷公藤红素对IL—1和IL—2活性及PGE2释放的抑制作用

雷公藤红素0.1～1.0μg/ml在试管内能降低LPS诱导的小鼠腹腔巨噬细胞外和细胞内白细胞介素-1(IL-1)的活性,也能抑制ConA诱导的小鼠脾细胞产生白细胞介素-2(IL-2).动态观察表明,雷公藤红素经预处理8h和3h后已能分别抑制IL-1和IL-2的产生。此外,雷公藤红素能降低A23187刺激家兔滑膜细胞释放前列腺素E_2(PGE_2)。     

A ring-enlarged oxetanocin A analogue as an inhibitor of HIV infectivity

Two ring-expanded analogues (compounds 2 and 3) of the anti-HIV fermentation product oxetanocin A (1) were synthesized from commercially available diacetone D-glucose. Antiviral testing against HIV in ATH8 cells revealed that the ring-expanded analogue 2 possessed a similar activity profile as oxetanocin A. Neither compound, however, was capable of providing full protection to the cells against HIV infection. The isomeric ring-expanded analogue 3 was totally devoid of anti-HIV activity. Molecular modeling suggested that while oxetanocin A and compounds 2 and 3 share a large common substructure with the potent anti-HIV drug, dideoxyadenosine (ddA), the extra hydroxymethyl substituent may contribute negatively to the binding of these molecules to a critical enzyme. The negative contribution may be less important in oxetanocin and isomer 2 than in isomer 3. From these studies it would appear that both oxetane and tetrahydrofuran rings are equivalent templates to support the adenine base in terms of anti-HIV activity.     

Szczepienia u dzieci z chorobą nowotworową − aktualne polskie zalecenia

The article presents, in accordance with current recommendations of the Infectious Diseases Society of America (IDSA) and the Programme of Immunization 2017 (PSO), proposals for the implementation of vaccination in children with cancer, depending on the applied treatment. We recommend to start vaccination 6 months after the end of cancer treatment, which is consistent with the guidelines of the IDSA. After vaccination with a live measles, mumps, rubella (Measles, Mumps, and Rubella, MMR), we recommend antibody level examination. In children treated with anti-CD20, we recommend vaccination after 6 months after completion of therapy. “Killed” vaccines can be administered 6 months after completion of cancer treatment. In the case of “live” vaccines, time of vaccination must be dependent on dose and time of administration of immunoglobulins.In children with autologous hematopoietic stem cell transplant (HSCT), we recommend vaccination at 6, and after allogeneic at 12 months after the transplant.Children after oncological treatment have an increased risk of viral and bacterial infections, particularly encapsulated bacteria; hence, be aware of vaccination against Haemophilus influenza, Streptococcus pneumoniae and Neisseria meningitidis.     

Effect of isosorbide dinitrate on neutrophil migration in vivo

The influence of isosorbide dinitrate on polymorphonuclear neutrophils migration into a sterile inflammatory focus was evaluated in 12 patients with ischemic heart disease. The number of neutrophils migrated into the "skin window" increased significantly during treatment with isosorbide. Also granulocyte clearance increased in comparison with control investigation. Possible clinical implications of this phenomenon are discussed.     

Oral bowenoid lesions: differential diagnosis and pathogenetic insights

OBJECTIVE: To determine if oral lesions exhibiting bowenoid features reflect the diverse microscopic appearance and biologic behaviour of Bowen's disease and bowenoid papulosis of the skin and genitalia. STUDY DESIGN: Seven cases of oral bowenoid lesions (6 with follow-up data) were assessed for differences in histologic features, human papillomavirus (HPV) viral status, and selected immunohistochemically detectable cell cycling proteins (p53, WAF-1, Cyclin D1, Bcl-2) and were correlated with available follow-up data. RESULTS: Two histologic subsets were identified. One, which was believed to correspond to Bowen's disease, exhibited large numbers of transepithelial apoptotic bodies, dyskeratotic cells and mitoses (bowenoid elements), poor differentiation of background epithelial cells, and consistent HPV-16/18 positivity. The other, believed to correspond to bowenoid papulosis, exhibited few bowenoid elements, good background differentiation, and inconsistent HPV-16/18 positivity. One of the aggressive cases exhibited repeated recurrences despite apparent total clinical excision, whereas none of the other group recurred. CONCLUSION: Although a small number of cases are in this study, results suggest that oral bowenoid lesions may exhibit histopathologic and behavioral variations ranging from oral Bowen's disease to oral bowenoid papulosis. Studies on more cases are needed to confirm this initial impression.     

Twenty years of Polish experience with three consecutive protocols for treatment of childhood acute myelogenous leukemia.

Until 1983, results of treatment of acute myelogenous leukemia (AML) in Poland with different regimens were very poor. In 1983, the Polish Pediatric Leukemia/Lymphoma Study Group introduced a unified treatment protocol--a modified version of BFM-83 protocol. This led to an increase in the curability of AML from 15% to approximately 32%. In 1994, a modification was made: the high-risk patients (>5% blasts in bone marrow on day 15 of therapy and all M5 cases) received two additional cycles with intermediate-dose cytarabine (ID-ARAC). This led to a nonsignificant improvement in the 5-year event-free survival (EFS) rate from 32 to 36%. A new treatment protocol employing idarubicin in place of daunorubicin was introduced in 1998 and produced better initial responses, increase in the number of patients attaining remission after induction therapy and proportional increase of standard-risk patients.The probability of 5-year EFS (pEFS) for the whole group of patients increased from 36 to 47%. In standard- and high-risk groups, the 5-year pEFS was 62 and 33%, respectively. The probability of 5-year disease-free survival was 58% in the whole group, and there were no differences between risk groups. Unsatisfactory treatment results in children classified into the high-risk group are principally due to the low remission rate.     

The effect of selected antiarrhythmic drugs on neutrophil free oxygen radicals production measured by chemiluminescence

Summary The evidence that free oxygen radicals produced by polymorphonuclear neutrophils (PMN) participate in generation of reperfusion arrhythmias is well documented. The in vitro effect of selected antiarrhythmic drugs on PMN free radicals production was evaluated by luminol- (LuCL) and lucigenin- (LgCL) amplified chemiluminescence stimulated with opsonized zymosan (o.z.) and phorbol myristate acetate (PMA). Fast sodium channel inhibitors varied in the influence on PMN chemiluminescence: from an inhibition in all models studied by procainamide, to lack of an effect by mexiletine. Propafenone, similarly to ajmaline and verapamil, inhibited LuCL stimulated with PMA, as well as LgCL after stimulation with both PMA and o.z. Bretylium tosylate decreased LuCL stimulated with both inducers, with no effect on LgCL. Amiodarone in high concentrations inhibited both LuCL and LgCL. -blockers propranolol and practolol impaired LuCL stimulated with o.z., as well as LgCL induced with PMA, whereas -blocker phentolamine inhibited LuCL and LgCL stimulated with both inducers. The drugs' effect on PMN free oxygen radicals production may constitute an additional mechanism of their activity.