HEALTH SEQUELAE OF TOBACCO EXPOSURE IN CHILDHOOD AND ADOLESCENCE

Tobacco consumption is one of the most common preventable cause of premature deaths worldwide. Persisting effects of exposure to tobacco smoke on children and adolescents are apparent during pregnancy and in early infancy, passive exposure to environmental tobacco smoke in home and elsewhere, and active smoking during adolescence. While, lung development in these stages of growth is not complete, tobacco smoke puts children and adolescents in danger of severe respiratory diseases and may interfere with the growth of their lungs. Active tobacco consumption by adolescents may have immediate adverse health outcomes such as addiction, impaired lung growth or reduced lung function. Much of the current evidence comes from longitudinal and cross-sectional longitudinal observational studies and propose that the strongest associations with smoke exposure are in the pregnancy and early childhood. The association of nicotine with respiratory system among children and adolescents is less clearly understood and the evidence primarily comes from in vitro and animal studies

Uloga pušenja i uzimanja alkoholnih pića u razvoju i ponavljanju plućne tuberkuloze

During a two-year period (2001-2003), 464 patients were treated for tuberculosis at Jordanovac Department for Lung Diseases in Croatia. Besides pulmonary tuberculosis in 97.7% of patients, patients were also treated for tuberculous pleurisy (0.9%), tuberculous laryngitis (0.6%), tuberculous meningitis (0.2%), tuberculous pericarditis (0.2%) and urogenital tuberculosis (0.4%). Out of the total number of patients, 57.3% declared themselves to be active smokers (men were predominant and made up to 80.8%) and 20.9% to be active alcohol consumers. Both risk factors, i.e. smoking and alcohol consumption, were present in 15.1% of all patients. The most common comorbidities were diabetes mellitus (30.4%), cardiac diseases (11.2%) and chronic obstructive pulmonary disease (8.0%). Lung carcinoma was the most common malignant disease (n=51), with Mycobacterium tuberculosis isolated in 33% of them. Seventy-two of 464 (15.5%) patients had recurrences of tuberculosis. Of these, 30.5% had one of the risk factors (20.8% were smokers and 9.7% consumed alcohol), while 32.5% of patients had both risk factors. In conclusion, cigarette smoking was proved to be the most significant risk factor for development of pulmonary tuberculosis and its recurrence.Tijekom dvije godine (2001.-2003.) u Klinici za plućne bolesti “Jordanovac”, Zagreb, Hrvatska, od tuberkuloze je liječeno 464 bolesnika. Osim najčešće plućne tuberkuloze u 97,7% bolesnika, oboljeli su liječeni i od eksudativnog tuberkuloznog pleuritisa (0,9%), laringealne tuberkuloze (0,6%), tuberkuloznog meningitisa (0,2%), perikardijalne tuberkuloze (0,2%) te tuberkuloze koja je zahvatila urogenitalni sustav (0,4%). Od ukupnog broja bolesnika 57,3% ih se izjasnilo kao aktivni pušači (muškarci 80,8%), dok je 20,9% deklarirano kao aktivni konzumenti alkohola. Ukupno je 15,1% bolesnika imalo oba rizična čimbenika u anamnezi, tj. i aktivno pušenje cigareta i konzumaciju alkohola. Od komorbiditeta najčešća je bila šećerna bolest u 30,4% bolesnika, od srčanih bolesti bolovalo je 11,2% bolesnika, dok je kronična opstruktivna plućna bolest bila prisutna u 8% bolesnika. Karcinom pluća bio je najčešće zastupljen među malignim bolestima. Od ukupnog broja oboljelih od karcinoma pluća (51 bolesnik), Mycobacterium tuberculosis izolirali smo u 33% bolesnika. Recidivi tuberkuloze su zabilježeni u 72 (15,5%) bolesnika. Jedan rizični čimbenik imalo je 30,5% bolesnika: pušača je bilo 20,8%, dok je alkohol konzumiralo 9,7% bolesnika, a 32,5% bolesnika imali su oba rizična čimbenika. Zaključno, pušenje cigareta pokazalo se kao najznačajniji rizični čimbenik za razvoj plućne tuberkuloze, kao i za pojavu recidiva tuberkuloze

RHD genotyping relevance in RhD negative blood donors

Cilj: RHD genotipizacijom odrediti vrstu i učestalost alela RHD koji uzrokuju serološki slabe D varijante u populaciji dobrovoljnih darivatelja krvi (DDK) u Hrvatskoj. Procijeniti osjetljivost seroloških metoda u otkrivanju slabog i/ili parcijalnog D antigena u skupini DDK kojima je D antigen dokazan indirektnom metodom, te razdiobu pojedinih varijantnih D alela u toj skupini. ----- Metode: Ukupno je obrađeno 6533 RhD negativnih DDK. Nakon izolacije genomske DNA u mješavini od 20 uzoraka, učinjen je RHD probir lančanom reakcijom polimeraze u stvarnom vremenu. Uslijedila je genotipizacija pomoću PCR-SSP metode korištenjem komercijalnih kitova (Inno-Train, Njemačka), te DNA sekvenciranje 6 uzoraka. U studiju je bilo uključeno i 263 DDK kojima je dokazan D antigen samo indirektnom metodom kojima je učinjena RHD genotipizacija i definiranje RHD polimorfizma. ----- Rezultati: Od 6533 RhD negativnih DDK, 23 nositelja gena RHD su potvrđena (0,35%), svi C/E pozitivni. Dvanaest uzoraka je reklasificirano kao RhD pozitivni. Izračunata frekvencija klinički značajnih D alela je bila 1: 543 (0,18%) u populaciji RhD negativnih DDK, ili 1:53(1,89%) kod C/E pozitivnih DDK. U populaciji DDK sa slabijom ekspresijom D antigena utvrđeno je 84,4% nositelja slabih D tipova 1, 2, 3, a najveća je učestalost slabog D tipa 1. ----- Zaključak: Istraživanje je otkrilo značajan broj D varijantnih alela u populaciji RhD negativnih DDK. Darivatelji krvi koji su ranije bili tipirani kao RhD negativni su reklasificirani kao RhD pozitivni i time je povećana sigurnost transfuzijskog liječenja.Aims: Determine the presence of RHD genes as well as the distribution of RHD alleles among RhD negative blood donors. Examine serologic accuracy in the detection of a weak and / or partial D antigen in donors with weak D antigen expression. ----- Methods: A total of 6,533 samples obtained from D-negative Croatian donors were screened for the presence of RHD by RT- PCR method. PCR-SSP was performed for D variants genotyping by using commercial genotyping kits (Inno-Train, Kronberg, Germany). The study also included 263 voluntary blood donors with weaker expression of D antigen confirmed by indirect method, who underwent RHD genotyping. ----- Results: 23 (0.35%) carriers of RHD alleles were identified. Twelve of them were redefined as RhD positive. The calculated frequency of clinically significant D alleles in RhD negative blood donors was 1:543(0.18%), or 1:53(1.89%) in C/E blood donors. Weak D type 1 was the most prevalent in the population of donors with weak D test positive. ----- Conclusion: The study revealed a significant number of D variant alleles in a population of RhD negative blood donors. Those once typed as RhD negative were reclassified as RhD positive, increasing the safety of transfusion therapy

RHD genotyping relevance in RhD negative blood donors

Cilj: RHD genotipizacijom odrediti vrstu i učestalost alela RHD koji uzrokuju serološki slabe D varijante u populaciji dobrovoljnih darivatelja krvi (DDK) u Hrvatskoj. Procijeniti osjetljivost seroloških metoda u otkrivanju slabog i/ili parcijalnog D antigena u skupini DDK kojima je D antigen dokazan indirektnom metodom, te razdiobu pojedinih varijantnih D alela u toj skupini. ----- Metode: Ukupno je obrađeno 6533 RhD negativnih DDK. Nakon izolacije genomske DNA u mješavini od 20 uzoraka, učinjen je RHD probir lančanom reakcijom polimeraze u stvarnom vremenu. Uslijedila je genotipizacija pomoću PCR-SSP metode korištenjem komercijalnih kitova (Inno-Train, Njemačka), te DNA sekvenciranje 6 uzoraka. U studiju je bilo uključeno i 263 DDK kojima je dokazan D antigen samo indirektnom metodom kojima je učinjena RHD genotipizacija i definiranje RHD polimorfizma. ----- Rezultati: Od 6533 RhD negativnih DDK, 23 nositelja gena RHD su potvrđena (0,35%), svi C/E pozitivni. Dvanaest uzoraka je reklasificirano kao RhD pozitivni. Izračunata frekvencija klinički značajnih D alela je bila 1: 543 (0,18%) u populaciji RhD negativnih DDK, ili 1:53(1,89%) kod C/E pozitivnih DDK. U populaciji DDK sa slabijom ekspresijom D antigena utvrđeno je 84,4% nositelja slabih D tipova 1, 2, 3, a najveća je učestalost slabog D tipa 1. ----- Zaključak: Istraživanje je otkrilo značajan broj D varijantnih alela u populaciji RhD negativnih DDK. Darivatelji krvi koji su ranije bili tipirani kao RhD negativni su reklasificirani kao RhD pozitivni i time je povećana sigurnost transfuzijskog liječenja.Aims: Determine the presence of RHD genes as well as the distribution of RHD alleles among RhD negative blood donors. Examine serologic accuracy in the detection of a weak and / or partial D antigen in donors with weak D antigen expression. ----- Methods: A total of 6,533 samples obtained from D-negative Croatian donors were screened for the presence of RHD by RT- PCR method. PCR-SSP was performed for D variants genotyping by using commercial genotyping kits (Inno-Train, Kronberg, Germany). The study also included 263 voluntary blood donors with weaker expression of D antigen confirmed by indirect method, who underwent RHD genotyping. ----- Results: 23 (0.35%) carriers of RHD alleles were identified. Twelve of them were redefined as RhD positive. The calculated frequency of clinically significant D alleles in RhD negative blood donors was 1:543(0.18%), or 1:53(1.89%) in C/E blood donors. Weak D type 1 was the most prevalent in the population of donors with weak D test positive. ----- Conclusion: The study revealed a significant number of D variant alleles in a population of RhD negative blood donors. Those once typed as RhD negative were reclassified as RhD positive, increasing the safety of transfusion therapy

RHD genotyping relevance in RhD negative blood donors

Cilj: RHD genotipizacijom odrediti vrstu i učestalost alela RHD koji uzrokuju serološki slabe D varijante u populaciji dobrovoljnih darivatelja krvi (DDK) u Hrvatskoj. Procijeniti osjetljivost seroloških metoda u otkrivanju slabog i/ili parcijalnog D antigena u skupini DDK kojima je D antigen dokazan indirektnom metodom, te razdiobu pojedinih varijantnih D alela u toj skupini. ----- Metode: Ukupno je obrađeno 6533 RhD negativnih DDK. Nakon izolacije genomske DNA u mješavini od 20 uzoraka, učinjen je RHD probir lančanom reakcijom polimeraze u stvarnom vremenu. Uslijedila je genotipizacija pomoću PCR-SSP metode korištenjem komercijalnih kitova (Inno-Train, Njemačka), te DNA sekvenciranje 6 uzoraka. U studiju je bilo uključeno i 263 DDK kojima je dokazan D antigen samo indirektnom metodom kojima je učinjena RHD genotipizacija i definiranje RHD polimorfizma. ----- Rezultati: Od 6533 RhD negativnih DDK, 23 nositelja gena RHD su potvrđena (0,35%), svi C/E pozitivni. Dvanaest uzoraka je reklasificirano kao RhD pozitivni. Izračunata frekvencija klinički značajnih D alela je bila 1: 543 (0,18%) u populaciji RhD negativnih DDK, ili 1:53(1,89%) kod C/E pozitivnih DDK. U populaciji DDK sa slabijom ekspresijom D antigena utvrđeno je 84,4% nositelja slabih D tipova 1, 2, 3, a najveća je učestalost slabog D tipa 1. ----- Zaključak: Istraživanje je otkrilo značajan broj D varijantnih alela u populaciji RhD negativnih DDK. Darivatelji krvi koji su ranije bili tipirani kao RhD negativni su reklasificirani kao RhD pozitivni i time je povećana sigurnost transfuzijskog liječenja.Aims: Determine the presence of RHD genes as well as the distribution of RHD alleles among RhD negative blood donors. Examine serologic accuracy in the detection of a weak and / or partial D antigen in donors with weak D antigen expression. ----- Methods: A total of 6,533 samples obtained from D-negative Croatian donors were screened for the presence of RHD by RT- PCR method. PCR-SSP was performed for D variants genotyping by using commercial genotyping kits (Inno-Train, Kronberg, Germany). The study also included 263 voluntary blood donors with weaker expression of D antigen confirmed by indirect method, who underwent RHD genotyping. ----- Results: 23 (0.35%) carriers of RHD alleles were identified. Twelve of them were redefined as RhD positive. The calculated frequency of clinically significant D alleles in RhD negative blood donors was 1:543(0.18%), or 1:53(1.89%) in C/E blood donors. Weak D type 1 was the most prevalent in the population of donors with weak D test positive. ----- Conclusion: The study revealed a significant number of D variant alleles in a population of RhD negative blood donors. Those once typed as RhD negative were reclassified as RhD positive, increasing the safety of transfusion therapy

Platelet Serotonin (5-HT) Concentration, Platelet Monoamine Oxidase B (MAO-B) Activity and HTR2A, HTR2C, and MAOB Gene Polymorphisms in Asthma

The complex role of the serotonin system in respiratory function and inflammatory diseases such as asthma is unclear. Our study investigated platelet serotonin (5-HT) levels and platelet monoamine oxidase B (MAO-B) activity, as well as associations with HTR2A (rs6314; rs6313), HTR2C (rs3813929; rs518147), and MAOB (rs1799836; rs6651806) gene polymorphisms in 120 healthy individuals and 120 asthma patients of different severity and phenotypes. Platelet 5-HT concentration was significantly lower, while platelet MAO-B activity was considerably higher in asthma patients; however, they did not differ between patients with different asthma severity or phenotypes. Only the healthy subjects, but not the asthma patients, carrying the MAOB rs1799836 TT genotype had significantly lower platelet MAO-B activity than the C allele carriers. No significant differences in the frequency of the genotypes, alleles, or haplotypes for any of the investigated HTR2A, HTR2C and MAOB gene polymorphisms have been observed between asthma patients and healthy subjects or between patients with various asthma phenotypes. However, the carriers of the HTR2C rs518147 CC genotype or C allele were significantly less frequent in severe asthma patients than in the G allele carriers. Further studies are necessary to elucidate the involvement of the serotonergic system in asthma pathophysiology