The history of Lapland : containing a geographical description, and a natural history of that country; with an account of the inhabitants, their original, religion, customs, habits, marriages, conjurations, employments, &c. Written by John Scheffer, ... Translated from the last edition in Latin, and illustrated with many curious copper-cutts. To which are added, the travels of the King of Sweden's mathematicians into Lapland: the history of Livonia, and the wars there: also a journey into Lapland, Finland, &c. Written by Dr. Olof Rudbeck in the year 1701

Added engraved title page: The history of Lapland.

Natural history of celiac disease-associated antibodies and progression to overt disease in children at increased genetic risk

Background: Celiac disease is a lifelong, gluten-sensitive, autoimmune-mediated chronic enteropathy, tightly associated with risk alleles at the HLA class II genes. Aims: This study was carried out as a part of the population-based Type 1 Diabetes Prediction and Prevention (DIPP) Project. The first aim was to study the natural history of celiac disease-associated antibodies before the diagnosis of celiac disease was made. The second aim was to describe when and in which order celiac disease-associated and type 1 diabetes-associated antibodies appeared in children with genetic risk for both diseases. Subjects and Methods: Antibodies against tissue transglutaminase (TGA) and other celiac disease-associated antibodies were measured in serum samples collected at 3- to 12-month intervals of children at genetic risk for celiac disease who participated in the DIPP project. Celiac disease was confirmed by duodenal biopsy. Type 1 diabetes-associated antibodies were measured in all samples that had been collected. Overt disease was diagnosed according to World Health Organization criteria. Follow-up continued until a diagnosis of type 1 diabetes or until the end of a defined follow-up period. Results: TGA appeared in children at genetic risk for celiac disease only after the first year of life, but anti-gliadin antibodies often emerged significantly earlier, at age 6 months. The data show that spontaneous disappearance of celiac disease-associated antibodies, transient or persisting, is a common phenomenon, at least in prepubertal children. In children with genetic susceptibility to type 1 diabetes and celiac disease, celiac disease-associated antibodies usually develop earlier than the type 1 diabetes-associated antibodies. Conclusions: The transient nature of celiac disease-associated antibodies emphasizes the significance of establishing seropositivity repeatedly in screening detected celiac disease before gastroscopy and duodenal biopsy are considered and emphasized the importance of duodenal biopsy for diagnosing celiac disease.

Molecular Markers of Oral Lichen Planus

Oral lichen planus (OLP) is a chronic inflammatory mucosal disease and is detected in between 0.5% - 2.2% of the population. WHO has defined OLP as a potentially precancerous disorder, representing a generalized state associated with a significantly increased risk of cancer. However, only 0.5 – 2.9% of OLP lesions will progress to cancer. Currently, there are no prognostic markers to identify the lesions at increased risk for malignant transformation. The main aim of these studies was to identify cellular and molecular markers in order to understand the pathogenesis of atrophic OLP and its progression towards malignancy. Selected markers for cell proliferation, adhesion, apoptosis, and lymphocytic infiltration were assessed by immunohistochemistry in addition to static cytometry analyses for DNA content. DNA quantification of epithelial cells in 82 biopsy samples derived from atrophic lichen planus showed altered DNA content in 41% of the samples. DNA content was associated with proliferation activity, topoisomerase IIalpha, desmocollin-1 and infection with human papillomavirus. CD27+ and CD38+ lymphocytes were detected in inflammatory cell infiltrate, indicating an abnormal homing of B cells from blood circulation to tissue. Physiologic cell death, apoptosis, is frequently seen in OLP, but its pathways are unknown. Here it was shown that caspases 2 and 12 were up-regulated in OLP, indicating that intracellular apoptosis, rather than an external causal factor, is triggering apoptosis. However, this thesis could not identify any singular prognostic marker of malignancy in OLP. Thus, every OLP patient should receive regular follow-up care to identify cancer risk patients at an early stage.

Försök, til en oeconomisk beskrifning, öfwer Satacunda häraders norra del : som innehåller anmärckningar i geographie, antiquiteter, physique, historia naturali, och oeconomie &c. Jemte nödige figurer. : Framgifwit af Pehr Adrian Gadd. Phil. mag.

Dedicated to: Konglige swenska wetenskaps academien.

Molecular markers for progression of squamous cell carcinoma of the skin

Incidence of nonmelanoma skin cancer (NMSC) is increasing. Ultraviolet (UV) –light is a major risk factor for the development of cutaneous SCC. Cutaneous SCCs that develop to chronic ulcers are known to progress and metastasize more easily than UV-induced SCCs. Matrix metalloproteinases (MMPs) are a group of proteolytic enzymes which are suggested to have a role in cancer growth and invasion. The molecular background for progression of cutaneous SCC was examined by immunohistochemistry (IHC) using tissue samples of recessive dystrophic epidermolysis bullosa (RDEB) –associated SCC, sporadic UV-induced SCC, and SCC precursors. IHC studies using tissue microarray (TMA) technique revealed overexpression of MMP-7 and MMP-13 in SCC tumor cells. MMP-7 expression was enhanced especially in the SCC tumor cells of the RDEB –associated SCCs. Studies with SCC cell lines showed that tumor cell derived MMP-7 activated heparin binding epidermal growth factor –like growth factor (HB-EGF) which enhanced the growth of SCC tumor cells. Further, it was shown that type VII collagen (COL7) is expressed in sporadic SCC tumor cells. Interestingly, it was shown that SCC –associated MMP-13 is capable of cleaving COL7 in vitro. COL7 cleavage may have a role in the progression of cutaneous SCC. Studies on serine proteinase inhibitor gene family using SCC tumor cell gene array, quantitative real-time PCR, SCC cell lines, normal human epidermal keratinocytes and IHC of TMA samples showed that serine proteinase inhibitor clade A, member 1 (serpinA1, alpha-1-antitrypsin) is expressed and produced by human SCC tumor cells but not by normal keratinocytes. Moreover, serpinA1 expression was shown to correlate with the progression of cutaneous SCC using transformed HaCaT-cell lines and mouse chemically induced skin SCC model. SerpinA1 may serve as a novel biomarker for the progression of cutaneous SCC. This study elucidated putative mechanisms of the progression of cutaneous SCC and revealed novel biomarker candidates for the progression of SCC of the skin.