Background: Type I diabetes is a chronic disease that places great demands on the child and family. Parental involvement has been found to be essential for disease outcome. However, fathers’ involvement has been less studied, even though high paternal involvement has been correlated with less disease impact on the family and higher quality of life among adolescents. Aim: The overall aim of the study was to explore and analyze constructions of fathers’ involvement in their child’s everyday life with type 1 diabetes from an ecological and health promotion perspective. Four specific aims were applied: 1) explore and describe discourses in health care guidelines for children with type 1 diabetes in Nordic countries, focusing on parents' positioning (I), 2) analyze how Swedish pediatric diabetes teams perceived and discussed fathers’ involvement in the care of their child with type 1 diabetes, and to discuss how the teams’ attitudes toward the fathers’ involvement developed during a focus group process (II), 3) explore and discuss how fathers involved in caring for their child with type 1 diabetes experience support from their pediatric diabetes team in everyday life with their child (III), and 4) analyze how involved fathers to children with type 1 diabetes understand their involvement in their child’s daily life and to discuss their perceptions from a health promotion perspective (IV). Material and methods: A qualitative and inductive approach was applied. Data were collected and analyzed during 2010-2012. The sample consisted of three pediatric guidelines originating from Norway, Denmark and Sweden (I), three Swedish pediatric diabetes teams (PDTs) (II), and 11 (III) and 16 (IV) fathers of children with type 1 diabetes who scored high involvement on the Parental Responsibility Questionnaire. Data were collected through repeated focus group discussions with the PDTs (II), online focus group discussions (III) and individual interviews (III, IV) with the fathers. Three analysis methods were applied: analysis of discourses (I), Constructivist Grounded Theory (II, III) and content analysis (IV). Findings: The findings illuminated the complex interaction between the pediatric guidelines, the PDTs and the fathers. Fathers highly involved in their child’s daily life experienced different levels of tension between the general recommendations and their personal experiences of living with a child with type 1 diabetes (III). The fathers regarded their involvement in their child’s diabetes care as additional to their general parenting, and a fine balance was identified between a health promotion perspective and a controlling involvement. The common denominator between the highly involved fathers was their use of parental leave (IV). The PDTs initially perceived fathers’ involvement as gendered and balanced on the mother’s agement, but as focus was set on fathers’ engagement the PDTs increased their awareness of this and started to identify and encourage their engagement II). At the macro-level, parents’ voices were diminished in Nordic pediatric diabetes guidelines in favor of an expert discourse (I). Conclusions: Fathers’ involvement concerning a child with type 1diabetes is constructed in a complex way, based on an interaction between the fathers’ perceptions of their additional involvement and the support provided by the PDTs; the PDTs’ perceptions of the fathers’ involvement; and how parents/fathers are constructed in pediatric diabetes guidelines. In order to promote the health and well-being of children with type 1 diabetes, fathers’ involvement needs to be taken into account in the pediatric guidelines as well as in clinical practice.

A method for designing low-density parity-check (LDPC) codes for bandwidth-efficient high-order coded modulation is proposed. Code structure utilizes the multi-edge-type LDPC code ensemble to achieve an improved match between codeword bit protection ca- pabilities and modulation bit-channel capacities over existing LDPC coded modulation techniques. The multi-dimensional EXIT vector field for the specific multi-edge parame- terization is developed for the analysis and design of code ensembles. A multi-dimensional EXIT decoding convergence condition is derived to enable efficient optimization. Code design results in terms of ensemble thresholds and finite-length Monte-Carlo simulations indicate that the new technique improves on the state-of-the-art performance, with sig- nificantly lower design and implementation complexity.

Impaired counterregulation during hypoglycemia in type 1 diabetes (T1D) is partly due to inadequate pancreatic islet alpha-cell glucagon secretion. We hypothesized that hypoglycemia can be prevented in autoimmune T1D by selective somatostatin receptor type 2 (SSTR2) antagonism of alpha cells to relieve SSTR2 inhibition, thereby increasing glucagon secretion. Diabetic biobreeding diabetes prone (BBDP) rats (D) vs non-diabetic BBDP (N) rats, underwent infusion of vehicle or SSTR2 antagonist (SSTR2a) during insulin-induced hypoglycaemia. D rats, treated with SSTR2a, needed little or no glucose to maintain hypoglycemia. To monitor real-time glucagon secretory response directly, we developed the technique of thin slices of the pancreas from D and N rats as well as normal human pancreas, subjected to perifusion with vehicle vs SSTR2a. SSTR2a treatment enhanced glucagon secretion in N and D rats and human pancreas. We conclude that SSTR2 antagonism can enhance hypoglycemia-stimulated glucagon release sufficient to achieve normoglycemic control.

Dietary proteins from Atlantic salmon and cod have previously been shown to have antidiabetic effects. Since dietary proteins are digested into small peptides before being absorbed through the intestinal mucosa, it is reasonable to deduce that the antidiabetic effect is due to enzymatically-digested peptides rather than the proteins themselves. The aim of this study was to develop a protocol to recover peptides with antidiabetic effects from salmon and cod protein digests and then scale up and optimize the salmon protein hydrolysate production process for industrial-scale production. The peptide mixtures were screened using cell culture assays for insulin-modulating activities and were further fractionated and purified for the final identification. Total yields of salmon and cod protein hydrolysates (<1 kDa) as measured by Kjeldahl nitrogen were 16.9% and 40.1%, respectively. The production process used for the salmon protein hydrolysate (<1 kDa) showed good reproducibility and potential for the industrial-scale production.

Hypoglycemia is one of the most serious acute complications in intensively treated diabetes. Recurrent hypoglycemia predisposes individuals to subsequent hypoglycemia, and diminished counterregulatory hormone responses increase this threat. Elevated pancreatic and/or circulating somatostatin has been reported in diabetic humans and animals, and we postulated that excessive somatostatin contributes to the attenuation of counterregulatory hormone release during hypoglycemia in diabetes. It is known that somatostatin suppresses stimulated secretion of glucagon, epinephrine, and corticosterone. We hypothesized that selective somatostatin receptor type 2 (SSTR2) antagonism would: (Study 1) improve hormone counterregulation to hypoglycemia, and (Study 2) ameliorate hypoglycemia in recurrently hypoglycemic rats. Using both high (10 U/kg) and low (5 U/kg) dose insulin to induce hypoglycemia, we demonstrate that inhibiting the action of somatostatin on SSTR2 normalizes the severely attenuated glucagon and corticosterone responses to acute hypoglycemia in diabetic rats. These improvements were specific to diabetes since SSTR2 antagonism did not increase these hormones in non-diabetic rats in response to hypoglycemia. In the absence of hypoglycemia, SSTR2 antagonist neither markedly alters glycemia nor causes sustained elevations in counterregulatory hormones in diabetic animals. Diabetic rats exhibit up to 65% and 75% more pancreatic and plasma somatostatin than non-diabetic rats following hypoglycemia, respectively. Despite improvements of glucagon and corticosterone, expression of gluconeogenic enzymes PEPCK1 and G6Pase was unaltered. SSTR2 antagonism reduced the glucose requirement during a hypoglycemic clamp induced with a lower dose of insulin. In recurrently hypoglycemic diabetic rats, we demonstrate that SSTR2 antagonist treatment reduces the depth and duration of hypoglycemia and promotes the recovery to euglycemia, without affecting the glycemia-lowering effect of insulin. This amelioration of hypoglycemia by SSTR2 antagonism may be attributable in part to the observed modest improvements of glucagon, epinephrine, and corticosterone counterregulation following recurrent hypoglycemia. These results implicate an important role for increased pancreatic, and possibly circulating, somatostatin in defective hypoglycemic counterregulation in diabetes.

A method for designing low-density parity-check (LDPC) codes for bandwidth-efficient high-order coded modulation is proposed. Code structure utilizes the multi-edge-type LDPC code ensemble to achieve an improved match between codeword bit protection ca- pabilities and modulation bit-channel capacities over existing LDPC coded modulation techniques. The multi-dimensional EXIT vector field for the specific multi-edge parame- terization is developed for the analysis and design of code ensembles. A multi-dimensional EXIT decoding convergence condition is derived to enable efficient optimization. Code design results in terms of ensemble thresholds and finite-length Monte-Carlo simulations indicate that the new technique improves on the state-of-the-art performance, with sig- nificantly lower design and implementation complexity.

Impaired counterregulation during hypoglycemia in type 1 diabetes (T1D) is partly due to inadequate pancreatic islet alpha-cell glucagon secretion. We hypothesized that hypoglycemia can be prevented in autoimmune T1D by selective somatostatin receptor type 2 (SSTR2) antagonism of alpha cells to relieve SSTR2 inhibition, thereby increasing glucagon secretion. Diabetic biobreeding diabetes prone (BBDP) rats (D) vs non-diabetic BBDP (N) rats, underwent infusion of vehicle or SSTR2 antagonist (SSTR2a) during insulin-induced hypoglycaemia. D rats, treated with SSTR2a, needed little or no glucose to maintain hypoglycemia. To monitor real-time glucagon secretory response directly, we developed the technique of thin slices of the pancreas from D and N rats as well as normal human pancreas, subjected to perifusion with vehicle vs SSTR2a. SSTR2a treatment enhanced glucagon secretion in N and D rats and human pancreas. We conclude that SSTR2 antagonism can enhance hypoglycemia-stimulated glucagon release sufficient to achieve normoglycemic control.

Successful pathogens like Pseudomonas syringae translocate type III effector proteins (T3SE) into host cells. Plant hosts react by specifically recognizing these effectors via R proteins that trigger defense responses. The T3SE family HopZ1 has evolved into three allelic forms as a result of diversifying selection. In this thesis, I investigated how virulence and immune-eliciting functions are determined in HopZ1a and HopZ1b in Arabidopsis. Mutational analysis of HopZ1a identified ten residues important for immune elicitation and at least three are involved in virulence functions. These results suggest that distinct key amino acid residues in HopZ1a mediate the two activities. The closely related HopZ1b T3SE elicits an inconsistent immune response in Arabidopsis. We found that HopZ1b-triggered immune response involves a TIR-type R protein and plastid-derived SA. Together, these results highlight an uncharacterized ETI response to the HopZ1 family of T3SEs.

Tottering and leaner mutant mice carry mutations in the pore-forming subunit (1A) of P/Q-type (CaV 2.1) voltage-gated calcium ion (Ca2+) channels that result in reduced Ca2+ current density. Since Ca2+ influx via voltage-dependent Ca2+ channels regulates important Ca2+-dependent neuronal processes including neurotransmitter release and synaptogenesis, we assessed effects of these mutations on hippocampus volume, neuronal density, neuronal morphology of hippocampal pyramidal cells in adult (six-month-old) mice, and adult neurogenesis in three-week-old and six-month-old mice. Hippocampal volume and neuronal density were assessed using hematoxylin and eosin stained serial sections. Neuronal morphology was assessed using Golgi-Cox staining as well as ultrastructural assessment using transmission electron microscopy. Adult hippocampal neurogenesis was assessed using standard 5-bromo-2’-deoxyuridine (BrdU) labeling with fluorescent immunohistochemistry (IHC) and proliferating cell nuclear antigen (PCNA) with diaminobenzidine IHC. To determine neuron and astrocyte survival, we used fluorescent double labeling for neurons with BrdU-neuronal nuclei IHC or astrocytes using BrdU-glial fibrillary acidic protein, respectively. Fluoro-Jade histochemistry was used to assess numbers of degenerating cells in the dentate gyrus subgranular zone. Decreased hippocampus volume was observed in tottering female mice and increased dentate hilar and CA1 cell density in mutant mice compared to wild type mice. Cell proliferation was increased in the hilus and combined CA3, CA2 and CA1 regions of mutant mice compared to wild type mice. Decreased total dendritic length and decreased number of dendritic intersections was observed in tottering mice compared to wild type mice. The decrease in dendritic arborization of tottering mice occurred at the concentric circles close to the neuronal cell body indicating that basal dendrites of CA1 pyramidal neurons are reduced. Taken together, P/Q-type voltage gated calcium channel mutation has age variable influence on adult hippocampal cell proliferation, and it altered neuronal morphology in terms of dendritic complexity in tottering mice, while the leaner mutation reduced mitochondrial density.

The project describes the development and standardization of the Myers-Briggs Type Indicator into the Greek language. Statistical properties of the Greek version were comparable to those of the original American version providing evidence of its adequacy as a psychometric tool. The comparison of the distribution of types of Greek university students (N = 946) with that of French Canadians, and Americans showed a preference for "thinking" and "perceiving". Further, gender associated preferences for thinking and feeling evident in the American and French Canadian norms were also present in the Greek data.