Specimen historicum de monumento Kiwikensi /

Mode of access: Internet.

Fo̊rsta grunderna i arabiska språket /

In Danish and Arabic.

Die geographisch-wissenschaftlichen ergebnisse meiner riesen in Zentralasien, 1894-1897.

Mode of access: Internet.

Svensk språklära, samt kort öfversigt af svenska språkets och litteraturens historia, till skolornas tjenst.

Mode of access: Internet.

Sveriges öde.

"En framstäilning av Sveriges politik under de sista fyra åren. Sedd mot världskrigets bakgrund."--Förord.

Finlands medicinal-författningar.

1.-4. de. compiled by Frans Johan Rabbe; 5.-7. del. by Alexander von Collan; 8.-del. by Karl Anders Bergstedt.

Inledning till isländska litteraturen och dess historia under medeltiden,

Mode of access: Internet.

Scholia vetera in Pindari carmina ...

Mode of access: Internet.

Untersuchungen uber Umlagerungen an der Nordseekuste, im besonderen an und auf den Insel Sylt.

Thesis (doctoral)--Friedrich-Alexanders-Universitat Erlangen.

Om en kvantitativ bestamning af varmevariationerna vid metalltraders dilatation och kompression.

Thesis (doctoral)--Upsala.

Ueber die loslichkeitsbeeinflussung in gemischten losungsmittel...

Thesis (doctoral)--

Swenska wetenskaps academiens handlingar.

Latest issue consulted: 4. ser., Band 9, Nr. 3, published in 1963.

Southern Tibet; discoveries in former times compared with my own researches in 1906-1908,

Mode of access: Internet.

Mannose-binding lectin gene polymorphism predicts hospital admissions for COPD infections

Infection frequently causes exacerbations of chronic obstructive pulmonary disease (COPD). Mannose-binding lectin (MBL) is a pattern-recognition receptor that assists in clearing microorganisms. Polymorphisms in the MBL2 gene reduce serum MBL levels and are associated with risk of infection. We studied whether the MBL2 codon 54 B allele affected serum MBL levels, admissions for infective exacerbation in COPD and disease susceptibility. Polymorphism frequency was determined by PCR-RFLP in 200 COPD patients and 104 smokers with normal lung function. Serum MBL was measured as mannan-binding activity in a subgroup of 82 stable COPD patients. Frequency of COPD admissions for infective exacerbation was ascertained for a 2-year period. The MBL2 codon 54 B allele reduced serum MBL in COPD patients. In keeping, patients carrying the low MBL-producing B allele had increased risk of admission for infective exacerbation (OR 4.9, P-corrected = 0.011). No association of MBL2 genotype with susceptibility to COPD was detected. In COPD, serum MBL is regulated by polymorphism at codon 54 in its encoding gene. Low MBL-producing genotypes were associated with more frequent admissions to hospital with respiratory infection, suggesting that the MBL2 gene is disease-modifying in COPD. MBL2 genotype should be explored prospectively as a prognostic marker for infection risk in COPD.

Effect of clarithromycin on nuclear factor-kappa B and transforming growth factor-beta in chronic rhinosinusitis

Objectives: Long-term, low-dose macrolide therapy is effective in the treatment of chronic rhinosinusitis. It is believed that macrolide antibiotics produce this benefit through an anti-inflammatory effect. In this study, the effect of clarithromycin treatment on the expression of transforming growth factor (TGF)-beta and the key pro-inflammatory nuclear transcription factor, NF-kappaB, was examined in vitro and in vivo. Study Design and Methods: In vitro: nasal mucosa was obtained from 10 patients with chronic sinusitis and was cultured for 24 hours in the presence of clarithromycin or control. Cellular expression of TGF-beta and NF-kappaB was determined by immunohistochemistry. In vivo: 10 patients with chronic rhinosinusitis were treated for 3 months with clarithromycin. Nasal mucosal biopsies were taken pre- and posttreatment. Cellular expression of TGF-beta and NF-kappaB was again determined by immunohistochemistry. Results: Clarithromycin, when applied to nasal biopsies in vitro, reduced cellular expression of TGF-beta and NF-kappaB. Nasal biopsies taken before and after clarithromycin treatment showed no differences in cellular expression of NF-kappaB or TGF-beta. Conclusion: Clarithromycin can reduce cellular expression of TGF-beta and NF-kappaB when applied in vitro, but its action during clinical therapy is less clear. Clarithromycin is capable of inhibiting pro-inflammatory cytokines in vitro, and reductions of TGF-beta and NF-kappaB may represent additional mechanisms by which macrolides reduce inflammation in chronic airway disease. Discrepancies between the actions of clarithromycin on nasal biopsies in vitro and after clinical therapy warrant further investigation.