Spelling suggestions: "subject:"insulinlike growth factor I"" "subject:"insulintekniken growth factor I""
91 |
Opposite associations of age-dependent insulin-like growth factor-I standard deviation scores with nutritional state in normal weight and obese subjectsSchneider, Harald Jörn, Saller, Bernhard, Klotsche, Jens, März, Winfried, Erwa, Wolfgang, Wittchen, Hans-Ulrich, Stalla, Günter Karl January 2006 (has links)
Objective: Insulin-like growth factor-I (IGF-I) has been suggested to be a prognostic marker for the development of cancer and, more recently, cardiovascular disease. These diseases are closely linked to obesity, but reports of the association of IGF-I with measures of obesity are divergent. In this study, we assessed the association of age-dependent IGF-I standard deviation scores with body mass index (BMI) and intra-abdominal fat accumulation in a large population.
Design: A cross-sectional, epidemiological study.
Methods: IGF-I levels were measured with an automated chemiluminescence assay system in 6282 patients from the DETECT study. Weight, height, and waist and hip circumference were measured according to the written instructions. Standard deviation scores (SDS), correcting IGF-I levels for age, were calculated and were used for further analyses.
Results: An inverse U-shaped association of IGF-I SDS with BMI, waist circumference, and the ratio of waist circumference to height was found. BMI was positively associated with IGF-I SDS in normal weight subjects, and negatively associated in obese subjects. The highest mean IGF-I SDS were seen at a BMI of 22.5–25 kg/m2 in men (+0.08), and at a BMI of 27.5–30 kg/m2 in women (+0.21). Multiple linear regression models, controlling for different diseases, medications and risk conditions, revealed a significant negative association of BMI with IGF-I SDS. BMI contributed most to the additional explained variance to the other health conditions.
Conclusions: IGF-I standard deviation scores are decreased in obesity and underweight subjects. These interactions should be taken into account when analyzing the association of IGF-I with diseases and risk conditions.
|
92 |
Prediction of incident diabetes mellitus by baseline IGF1 levelsSchneider, Harald Jörn, Friedrich, Nele, Klotsche, Jens, Schipf, Sabine, Nauck, Matthias, Völzke, Henry, Sievers, Caroline, Pieper, Lars, März, Winfried, Wittchen, Hans-Ulrich, Stalla, Günter Karl, Wallaschofski, Henri January 2011 (has links)
Objective: IGF1 is associated with metabolic parameters and involved in glucose metabolism. Low-IGF1 has been implicated in the etiology of glucose intolerance and subjects with pathological causes of either low- or high-IGF1 are at risk of diabetes. We hypothesized that both low- and high-IGF1 levels increase the risk of diabetes and aimed to assess the role of IGF1 in the risk of developing diabetes in a large prospective study.
Design: An analysis of two prospective cohort studies, the DETECT study and SHIP.
Methods: We measured IGF1 levels in 7777 nondiabetic subjects and assessed incident diabetes mellitus during follow-up.
Results: There were 464 cases of incident diabetes during 32 229 person-years (time of follow-up in the DETECT study and SHIP: 4.5 and 5 years respectively). There was no heterogeneity between both studies (P>0.4). The hazard ratios (HRs) of incident diabetes in subjects with IGF1 levels below the 10th or above the 90th age- and sex-specific percentile, compared to subjects with intermediate IGF1 levels, were 1.44 (95% confidence interval (CI) 1.07–1.94) and 1.55 (95% CI 1.06–2.06) respectively, after multiple adjustment. After further adjustment for metabolic parameters, the HR for low-IGF1 became insignificant. Analysis of IGF1 quintiles revealed a U-shaped association of IGF1 with risk of diabetes. Results remained similar after exclusion of patients with onset of new diabetes within 1 year or with borderline glucose or HbA1c levels at baseline.
Conclusions: Subjects with low- or high-IGF1 level are at increased risk of developing diabetes.
|
93 |
Notch-1 and IGF-1 as Survivin Regulatory Pathways in Cancer: A DissertationLee, Connie Wing-Ching 04 June 2008 (has links)
The 21st century brought about a dramatic increase in knowledge about genetic and molecular profiles of cancer. This information has validated the complexity of tumor cells and increased awareness of “nodal proteins”, but has yet to advance the development of rational targeted cancer therapeutics. Nodal proteins are critical cellular proteins that collect biological inputs and distribute the information across diverse biological processes. Survivin acts as a nodal protein by interfacing the multiple signals involved in mitosis and apoptosis and functionally integrate proliferation, cell death, and cellular homeostasis. By characterizing survivin as a target of both Type 1 Insulin-like Growth Factor (IGF-1) and Notch developmental signaling, we contribute to the paradigm of survivin as a nodal protein. The two signaling systems, Notch and IGF-1, regulate survivin by two independent mechanisms. Notch activation induces survivin transcription preferentially in basal breast cancer, a breast cancer subtype with poor prognosis and lack of molecular therapies. Activated Notch binds the transcription factor RBP-Jк and drives transcription from the survivin promoter. Notch mediated survivin expression increases cell cycle kinetics promoting tumor proliferation. Inhibition of Notch in a breast xenograft model reduced tumor growth and systemic metastasis. On the other hand, IGF-1 signaling drives survivin protein translation in prostate cancer cells. Binding of IGF-1 to its receptor activates downstream kinases, mammalian target of rapamycin (mTOR) and p70 S6 protein kinase (p70S6K), which modulates survivin mRNA translation to increase the apoptotic threshold. The multiple roles of survivin in tumorigenesis implicate survivin as a rational target for the “next generation” of cancer therapeutics.
|
94 |
An Insulin-Like Growth Factor-I Receptor Defect Associated with Short Stature and Impaired Carbohydrate Homeostasis in an Italian PedigreeMohn, Angelika, Marcovecchio, Maria Loredana, de Giorgis, Tommaso, Pfaeffle, Roland, Chiarelli, Francesco 27 July 2022 (has links)
Mutations in the insulin-like growth factor-I
(IGF-I) receptor (IGF1R) have been associated with prenatal
and postnatal growth retardation. However, little is known about potential effects of mutations in the IGF1R on carbohydrate
homeostasis. Methods: We investigated clinical, endocrine
and metabolic parameters in four family members
carrying a novel IGF1R mutation (p.Tyr387X): an 18-year-old
male (index case), his sister and two paternal aunts. Results:
All family members showed a variable degree of impairment
in prenatal growth, with birth weight standard deviation
scores (SDS) between –1.65 and –2.37 and birth length SDS
between –1.78 and –3.08. Their postnatal growth was also
impaired, with height SDS between –1.75 and –4.86. The index case presented high IGF-I levels during childhood and
adolescence and delayed bone age. The index case and his
two paternal aunts had impaired glucose tolerance (IGT) associated
with a variable degree of alterations in insulin sensitivity
and secretion. In contrast, the index case’s sister, who
had had IGT during pregnancy, showed normal glucose metabolism
but reduced insulin sensitivity. Conclusion: This is
the first study showing an association between a novel IGF1R
mutation and a variable degree of alterations in prenatal and
postnatal growth and in carbohydrate metabolism.
|
95 |
In Vitro Binding and Transport Regulation by Endothelial Cells: Preliminary Studies looking at FIX and IGF-ISutton, Amanda 13 April 2005 (has links)
Endothelial cells separate the bloodstream from the underlying tissue and play a crucial role in vascular homeostasis. They also form an important barrier for vascular drug delivery. This thesis contains preliminary studies targeted at understanding the mechanisms of binding and transport across endothelial cells cultured in vitro. Specifically, the first study investigates how the recombinant source of Factor IX (FIX), a blood coagulant protein used in the treatment of Hemophilia B, impacts surface ligand binding (FIX to its specific receptors) to bovine aortic endothelial cells (BAECs). Competitive binding experiments between 125I-FIX and FIX were undertaken to quantify the interaction of recombinant and transgenic FIX with BAECs and human collagen IV and determine if there was a measurable difference in binding affinity. Results indicate limited specific binding of 125I-FIX to BAECs and no binding to human collagen IV. Concrete conclusions were not drawn from this data due to technical issues during the experimental process. The second study investigates insulin-like growth factor-I (IGF-I) transport across both BAEC and MAC-T cells, a mammary epithelial cell line, cultured on tissue culture inserts. IGF-I is a circulatory growth factor implicated in the regulation of cell division and tissue proliferation. Competitive binding experiments between 125I-IGF-I and unlabeled protein (IGF-I, Y60L-IGF-I, a mutant of IGF-I, and IGF Binding Protein-3 (IGFBP-3)) were undertaken to quantify the binding and transport of IGF-I under various experimental conditions. Results confirmed earlier work from the Williams' laboratory indicating that 125I-IGF-I transport was enhanced by incubation with its non-receptor-binding analog, Y60L-IGF-I, but cell surface associated 125I-IGF-I was decreased by its presence. Other studies were undertaken but conclusive results could not be drawn. / Master of Science
|
96 |
Quantification of the Binding of Insulin-like Growth Factor-I (IGF-I) and IGF Binding Protein-3 (IGFBP-3) Using Surface Plasmon ResonanceCassino, Theresa Rachel 20 June 2002 (has links)
Insulin-like growth factor-I is a small growth factor known to signal in a variety of mammalian cells through the IGF-I cell surface receptor (IGF-IR). A unique feature of the IGF-I system is the regulation of this binding by soluble IGF binding proteins. Recent studies from our laboratory show that there is a pH dependence in the association of IGF-I with the cell surface in the presence of IGFBP-3 which suggested increased association of IGF-I with IGFBP-3 at low pH. We studied cell free interaction of IGF-I and IGFBP-3 as a function of pH using surface plasmon resonance (SPR) in order to understand the mechanism that causes the increased association. In our studies three different SPR instruments with different surfaces for immobilization of one of the binding partners were used: a Leica Bio-SPR 9000 with a low molecular weight carboxymethylated dextran (CMD) surface, a BIAcore 2000 with a high molecular weight CMD surface and a Leica SPR 2001 Alpha with a planar mixed self-assembled monolayer (mSAM) surface. Since the experimental system we used was transport sensitive, only the mSAM surface, under optimized conditions, produced results that fit to a single site model. Results suggest that use of CMD layers for immobilization of one partner of a high-affinity binding complex can result in transport limited binding for which simple analysis is inappropriate. Future studies are planned to expand the work with the mSAM surface to elucidate whether a significant difference between the binding parameters as a function of pH exists. / Master of Science
|
97 |
Estudio en poblaciones seleccionadas de la fiabilidad de nuevos protocolos de detección de consumo de hormonas recombinantes (hgH y EPO)Abellán Sánchez, María Rosario 07 July 2006 (has links)
Las hormonas recombinantes eritropoyetina (EPO) y hormona de crecimiento (GH), prácticamente iguales a las endógenas y de corta vida media en circulación, son de difícil detección directa en el control antidopaje. Se determinaron los valores poblacionales de los biomarcadores indirectos EPO, receptor soluble de la transferrina, insulin-like growth factor-I (IGF-I) y procolágeno tipo III péptido (P-III-P), en poblaciones seleccionadas de deportistas, y el efecto del ejercicio y los distintos tipos de entrenamiento sobre su concentración sérica. La comparación de resultados obtenidos mediante distintos ensayos demostró la necesidad de una validación exhaustiva previa a su utilización. A excepción del P-III-P, los biomarcadores séricos propuestos para la detección de rhEPO y rhGH no se encuentran directamente afectados por el nivel atlético, el ejercicio o la distinta carga de entrenamiento realizada a lo largo de la temporada deportiva. La edad es la principal influencia sobre las concentraciones séricas de IGF-I y P-III-P. / Direct detection of recombinant peptidic hormones erythropoietin (EPO) and growth hormone (GH), very similar to endogen molecules and with a short half life in blood, is difficult in antidoping control. The main objective of this work is to determine indirect biomarkers' values of EPO, soluble transferrin receptor, insulin-like growth factor-I (IGF-I) and procollagen type III peptide (P-III-P), in selected populations of athletes, and the effect of exercise and different types of training on their concentration in serum. The comparison of results obtained by the different assays showed the need of extensive validation of the analytical techniques before their use in the antidoping field. Excepting P-III-P, proposed biomarkers for the detection of rhEPO and rhGH abuse are not directly influenced by the athletic level, exercise or different training workload along the sport season. Age is the main factor affecting IGF-I and P-III-P concentrations in serum.
|
98 |
Nutritional status before and during pregnancy in relation to the maternal insulin-like growth factor-system and health related variables in the offspring : studies in women, guinea pigs and rats /Olausson, Hanna, January 2004 (has links) (PDF)
Diss. (sammanfattning) Linköping : Univ., 2004. / Härtill 6 uppsatser.
|
99 |
Efeito do fator de crescimento insulina-símile-I em promastigota e amastigota intracelular de Leishmania (Viannia) braziliensis de pacientes com diferentes formas clínicas de leishmaniose tegumentar americana / Effect of Insulin-like growth factor-I on promastigotes and intracellular amastigotes of Leishmania (Viannia) braziliensis from patients with different clinical forms of American tegumentary leishmaniasisSouza, Luana Dias de 03 October 2012 (has links)
Leishmanioses são doenças causadas por protozoários do gênero Leishmania e se apresentam sob forma tegumentar ou visceral. No Brasil, a leishmaniose tegumentar americana (LTA) é causada, na sua maioria, por Leishmania (Viannia) braziliensis e conhecem-se principalmente as formas cutânea (LC), mucosa (LM) e disseminada (LD) da doença. Na LTA as formas clínicas tem sido atribuídas a diferenças na resposta imune do hospedeiro, mas recentemente vinculam-se também à variabilidade intraespecífica da L. (V.) braziliensis. Neste estudo avaliamos se haveria variabilidade biológica nos isolados de L. (V.) braziliensis, provenientes de pacientes com LC, LM e LD, principalmente em resposta a fator de crescimento insulina-símile-I (IGF-I). Os fatores de crescimento do hospedeiro tem sido alvo de estudos no desenvolvimento das leishmanioses, sendo IGF-I um deles. Havíamos demonstrado em estudos anteriores, utilizando Leishmania (Leishmania) amazonensis, que IGF-I induz proliferação, aumentando a atividade da arginase, com geração de poliaminas e diminuindo a síntese de óxido nítrico. No presente estudo analisamos o efeito de IGF-I em L.(V.) braziliensis, espécie prevalente no Brasil. Avaliamos inicialmente as características dos diferentes isolados enquanto promastigota e no prosseguimento enquanto amastigota em células de linhagem monocítica humana THP-1, com e sem estímulo de IGF-I. Nossos dados sugerem que há diferenças na atividade da arginase basal entre os isolados de L. (V.) braziliensis, sendo maior naqueles provenientes de pacientes com LM. IGF-I aumentou a atividade da arginase nos isolados de LC e LD, mas não de LM. Nos isolados em forma amastigota nas células de linhagem monocítica humana THP-1, o efeito de IGF-I foi de aumento do parasitismo nos isolados de LC e LM e de diminuição com os de LD. Nos isolados de LD a atividade da arginase basal foi menor que nos de LC. Por outro lado, a produção de óxido nítrico tendeu a ser maior em isolados de LD quando sob estímulo de IGF-I. Os dados sugerem que diferenças nas características biológicas dos parasitos podem contribuir na apresentação clínica dos casos da LTA. / Leishmaniasis are diseases caused by protozoa of the genus Leishmania that may manifest as cutaneous or visceral disease. In Brazil, American tegumentary leishmaniasis (ATL) is caused mostly by Leishmania (Viannia) braziliensis and cutaneous (CL), mucosal (ML) and disseminated (DL) forms of the disease are known.The diversity of clinical manifestations has been attributed to differences in the host immune response, but recently it has also been related to intraspecific variability of L. (V.) braziliensis. In the present study we evaluated whether there were biological variability in different isolates of L. (V.) braziliensis from patients with CL, ML, and DL, mainly in response to insulin-like growth factor-I (IGF-I). Growth factors of the host have been investigated in the development of leishmaniasis including IGF-I. In previous studies using Leishmania (Leishmania) amazonensis IGF-I was shown to induce proliferation, to increase the activity of arginase, generating polyamines and to decrease the synthesis of nitric oxide. In this study we analyzed the effect of IGF-I in L. (V.) braziliensis, a species prevalent in Brazil. Initially we evaluated the characteristics of individual isolates as promastigote and further as amastigote within human macrophage cell line THP-1 with and without IGF-I stimulation. Our data suggest that there are differences in the basal arginase activity amongst isolates of L. (V.) braziliensis, being higher in those from patients with ML. IGF-I increased the activity of arginase in the isolates of CL and DL, but not of ML. In isolates in the form of amastigotes within THP-1 cells, IGF-I induced the increase of parasitism of isolates from CL and ML, and decrease of those from DL. In isolates of DL the basal arginase activity was lower than in those of CL. Moreover, the production of nitric oxide tended to be higher with isolates of DL upon IGF-I stimulation. The data suggest that differences in the biological characteristics of parasites may contribute to the diversity of clinical presentation of ATL.
|
100 |
Insulin-like growth factor-1 to improve neurological recovery after acute spinal cord injury: a porcine study.January 2012 (has links)
研究目的:脊髓損傷是中樞神經系統的嚴重創傷,致殘率高。脊髓損傷後的再生修復一直是當前醫學的難題。迄今為止,脊髓損傷依然缺乏一種有效地治療方法。既往研究證明,胰島素樣生長因子-1對鼠和兔脊髓損傷有保護作用,為了進一步把這些發現應用到臨床方面,我們採用與人類生理更相近的豬只作為實驗動物,構建與臨床相似的脊髓損傷動物模型,并以此為基礎,系統性研究胰島素樣生長因子-1的脊髓保護作用,評估該治療的功效。 / 研究方法:以運動誘發電位為指導,通過直接壓迫和牽拉造成脊髓損傷。18頭猪只隨機分為3組:胰島素樣生長因子-1治療組、生長激素治療組及生理鹽水對照組。脊髓損傷后1小時、24小時及48小時經鞘內注射給藥。于術後第1天、第3天及第21天收集腦脊液檢測胰島素樣生長因子-1和生長激素濃度。連續21天使用修正的 Tarlov 評分標準對動物的運動功能進行評估。第21天處死動物並取材,檢測脊髓中NeuN, GFAP, caspase-3 的活性,并通過TUNEL染色觀察細胞凋亡情況,比較各組之間有無差別。 / 研究結果:通過這種方法建立的脊髓損傷動物模型穩定可靠,各組之間無明顯差異。鞘內給藥24小時及48小時后,腦脊液中胰島素樣生長因子-1和生長激素濃度明顯升高,術後21天檢測,其濃度恢復至基礎值。胰島素樣生長因子-1治療組的運動功能的恢復優於其它各組。與生理鹽水對照組比較,胰島素樣生長因子-1治療組可以明顯提高脊髓損傷后神經元的存活數量,抑制星形膠質細胞增生,減少細胞凋亡。而生長激素治療組僅抑制星形膠質細胞增生,其它方面與生理鹽水對照組無明顯差別。 / 結論:胰島素樣生長因子-1通過提高神經元存活數量,抑制星形膠質細胞增生,以及減少細胞凋亡促進脊髓損傷的恢復。 / Objective: Spinal cord injury is a devastating condition that leads to long-term disabilities. Currently, there is no effective treatment that minimizes spinal cord damage or enhances neurological recovery. Recent studies in rats or rabbits suggested that neurologic recovery after spinal cord injury could be improved with the administration of neurotropic hormones, such as insulin-like growth factor-1 (IGF-1). In order to apply such bench-side discovery to clinical practice, we conducted a study in a higher animal model, akin to human physiology, to evaluate the effectiveness of intrathecal injections of IGF-1to improve neurological recovery in a porcine model of acute traumatic spinal cord injury. / Methods: Traumatic spinal cord injury model was produced by controlled compression and distraction of the exposed T12 segment of the spinal cord. Eighteen pigs were randomly assigned to receive intrathecal injections of either IGF-1, growth hormone or saline at 1, 24 and 48 hours after spinal cord injury. Locomotor function was assessed daily using the validated modified Tarlov’s scale for 21 days. Spinal cord segments were then harvested and the survival of neurons, reactive astrogliosis and apoptosis were determined using neuronal-specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP), cleaved caspase-3 and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assays. / Results: Intrathecal injections of IGF-1 and growth hormone significantly increase the concentrations of the neurotropic hormones in the cerebrospinal fluid after injury (p < 0.01). These concentrations returned to baseline by 21 days after drug delivery. Motor deficits on the first day after injury were comparable between animals in the treatment and control groups. By the end of the third week, neurologic recovery was better in animals receiving IGF-1 treatment (p < 0.05). Immunohistological and western blot studies of the injured segments of spinal cord showed that treatment with both IGF-1 and growth hormone prevented reactive astrogliosis (p < 0.05) while only IGF-1 improved the survival of mature neurons (p < 0.05). IGF-1 also inhibited apoptosis after spinal cord injury (p < 0.05). / Conclusions: In our clinically relevant model of traumatic spinal cord injury in pigs, intrathecal injection of IGF-1 demonstrated beneficial effects on neurological and histological recovery. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Wang, Qinzhou. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 105-122). / Abstract also in Chinese. / Declaration of origination --- p.I / Abstract --- p.II / Acknowledgements --- p.VI / Table of Contents --- p.VIII / List of Tables --- p.XII / List of Figures --- p.XIII / Abbreviations --- p.XVIII / Chapter Part 1 --- Spinal Cord Injury: A Review --- p.1 / Chapter Chapter 1-1 --- Acute Spinal Cord Injury: Epidemiology, Socioeconomic Impact --- p.2 / Chapter 1.1.1 --- Epidemiology of Spinal Cord Injury --- p.2 / Chapter 1.1.2 --- Socioeconomic Impact of Acute Spinal Cord Injury --- p.5 / Chapter Chapter 1-2 --- Mechanisms of Spinal Cord Injury --- p.6 / Chapter Chapter 1-3 --- Putative Treatments for Spinal Cord Injury --- p.8 / Chapter 1.3.1 --- Methylprednisolone --- p.8 / Chapter 1.3.2 --- Stem Cell Therapy --- p.11 / Chapter 1.3.3 --- Riluzole --- p.11 / Chapter 1.3.4 --- Other Pharmacological Therapies for Spinal Cord Injury --- p.12 / Chapter Chapter 1-4 --- Insulin-like Growth Factor-1 for the Treatment of Spinal Cord Injury --- p.13 / Chapter Chapter 1-5 --- Summary --- p.17 / Chapter Part 2 --- Insulin-like Growth Factor-1 and Growth Hormone for Spinal Cord Injury --- p.18 / Chapter Chapter 2-1 --- Hypothesis and Objectives --- p.19 / Chapter Chapter 2-2 --- Establishment of Animal Models for Acute Spinal Cord Injury --- p.22 / Chapter 2.2.1 --- Introduction --- p.22 / Chapter 2.2.2 --- Experimental Animals --- p.22 / Chapter 2.2.3 --- Anesthesia --- p.23 / Chapter 2.2.4 --- Transcranial Electrical Motor Evoked Potential --- p.26 / Chapter 2.2.5 --- Surgery --- p.28 / Chapter 2.2.6 --- Statistics --- p.34 / Chapter 2.2.7 --- Results --- p.34 / Chapter 2.2.8 --- Discussion --- p.38 / Chapter Chapter 2-3 --- Optimal Stimulation Protocols for Transcranial Electrical Motor Evoked Potential. --- p.42 / Chapter 2.3.1 --- Introduction --- p.42 / Chapter 2.3.2 --- Methods --- p.42 / Chapter 2.3.2.1 --- Experimental Animals and Anesthesia --- p.42 / Chapter 2.3.2.2 --- Transcranial Electrical Motor Evoked Potential Recording --- p.44 / Chapter 2.3.2.3 --- Stimulation Protocol --- p.44 / Chapter 2.3.3 --- Analyses --- p.44 / Chapter 2.3.4 --- Results --- p.45 / Chapter 2.3.5 --- Discussion --- p.52 / Chapter Chapter 2-4 --- Evaluation of the Efficacy of Insulin-like Growth Factor-1 and Growth Hormone in a Porcine Model --- p.54 / Chapter 2.4.1 --- Introduction --- p.54 / Chapter 2.4.2 --- Materials and Methods --- p.54 / Chapter 2.4.2.1 --- Study Design --- p.54 / Chapter 2.4.2.2 --- Intrathecal Injection and Collection of Cerebrospinal Fluid --- p.58 / Chapter 2.4.2.3 --- Measurements --- p.58 / Chapter 2.4.2.3.1 --- Clinical Evaluation --- p.58 / Chapter 2.4.2.3.2 --- Biochemical Assessments --- p.58 / Chapter 2.4.2.3.3 --- Spinal Cord Section, Histological and Immunochemical Staining --- p.63 / Chapter 2.4.2.3.4 --- Western Blot --- p.69 / Chapter 2.4.3 --- Statistical Analysis and Sample Size Calculation --- p.72 / Chapter 2.4.3.1 --- General Analysis --- p.72 / Chapter 2.4.3.2 --- Sample Size --- p.72 / Chapter 2.4.4 --- Results --- p.73 / Chapter 2.4.4.1 --- Changes of TceMEP --- p.73 / Chapter 2.4.4.2 --- Motor Deficit after Spinal Cord Injury at Baseline --- p.75 / Chapter 2.4.4.3 --- Insulin-like Growth Factor-1 and Growth Hormone in Cerebrospinal Fluid --- p.77 / Chapter 2.4.4.4 --- Clinical Assessment --- p.80 / Chapter 2.4.4.5 --- Demyelination, Neuron Survival and Astrocyte Reaction --- p.85 / Chapter 2.4.4.6 --- Apoptosis --- p.89 / Chapter 2.4.5 --- Discussion --- p.93 / Chapter 2.4.5.1 --- Principal Findings --- p.93 / Chapter 2.4.5.2 --- Insulin-like Growth Factor-1 and Neuroprotection after Spinal Cord Injury --- p.93 / Chapter 2.4.5.3 --- Growth Hormone and Neuroprotection after Spinal Cord Injury --- p.95 / Chapter 2.4.5.4 --- Strengths and Limitations of Our Study --- p.96 / Chapter 2.4.5.5 --- Summary --- p.97 / Chapter Part 3 --- Summary and Future Directions --- p.99 / Chapter Chapter 3-1 --- Summary --- p.100 / Chapter Chapter 3-2 --- Future Directions --- p.103 / Chapter Part 4 --- References and appendixes --- p.104 / References --- p.105 / Appendixes --- p.123
|
Page generated in 0.0572 seconds