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- Ahmad, Tashfeen
(author)
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Diabetic osteopathy : a study in the rat
- 2003
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Doctoral thesis (other academic/artistic)abstract
- The present study on non-obese Goto-Kakizaki (GK) rats with type-2 diabetes and neuropathy was an attempt to describe and define pertinent features of diabetic osteopathy. Altogether, the study included 33 GK rats aged 12 and 20 months, and 36 age-matched Wistar rats as controls. All underwent test of glucose tolerance and nerve (sciatic) conduction velocity (NCV) showing that the diabetic rats had significantly higher blood glucose levels and lower NCV confirming the presence of diabetes and neuropathy. Skeletal features: Radiologic analysis of bone entailed X-ray, Dual Energy X-ray Absorptiometry (DEXA) and peripheral Quantitative Computed Tomography (pQCT). In diabetic rats, the length of humerus and height of vertebrae was reduced by 8%. The long bones exhibited endosteal erosion of the diaphyses up to 18% and periosteal expansion up to 8%. The vertebrae and metaphyses of long bones showed a decrease up to 24% in areal bone mineral density (BMD), whereas no decrease was seen in the diaphyses. Cross-sectional measurements by pQCT showed a decrease in volumetric BMD ranging from 33 to 62%, which exclusively pertained to trabecular bone (vertebrae, metaphyses), whereas volumetric BMD of the cortical bone of diaphyses was only marginally affected. The results indicate that juxta-articular bone in diabetes is substantially weaker, whereas diaphyseal cortical bone may be even stronger. Over all, the observations suggest that the diabetic skeleton is characterized by regional changes, which cannot be explained by systemic factors like calcium regulating hormones. Local bone turn-over is regulated by complex mechanisms involving cytokines, prostaglandins, growth factors and, also neuropeptides. Further analysis focused on the insulin-like growth factor (IGF) system and neuronal mediators in bone. IGF system: Immunoassays of IGF-I were done on serum, ankle samples and cortical preparations. In addition, the inhibitory IGF-I binding proteins, IGFBP-1 and -4 were analysed in serum. In diabetic rats, serum IGF-I was reduced by 18%, while IGFBP-1 and IGFBP-4 were increased by 89 and 20%, respectively. This complies with the lower BMD in the diabetic rats. In cortical bone, IGF-I was reduced by 38%, whereas no change was seen in ankles. The loss of IGF-I in cortical bone represents a novel finding. Given the cortical expansion observed in diabetic rats, the opposite was expected. Conceivably, loss of IGF-I results in endosteal erosion, which is compensated by periosteal expansion. Neuropeptides: The analyses focused on two sensory mediators, i.e. substance P (SP) and calcitonin gene- related peptide (CGRP), and one autonomic, i.e. neuropeptide Y (NPY). Immunohistochemistry was applied to ankles and tibial diaphyses, whereas radioimmunoassay (RIA) was used for separate preparations of periosteum, cortex and bone marrow from femur and tibia, whole ankles, dorsal root ganglia (DRG) and lumbar spinal cord. The morphological analysis showed SP, CGRP and NPY positive nerve fibers in bone and joints, which mostly were blood vessel related, although free terminals were also seen. In addition, NPY-positive hematopoietic cells were observed in the bone marrow. RIA revealed a significant decrease of CGRP, albeit not of SP, in DRG (-26%) and spinal cord (-29%) in the diabetic rats. As for bone, only NPY was significantly reduced, most evidently in bone marrow (-66%), but also in cortical bone (-36%) and ankles (-29%). Given the bone anabolic effects of CGRP and NPY, loss of these neuropeptides may prove, at least partly, to underlie the trabecular osteopenia and endocortical erosion observed in diabetic rats. Conclusion: The skeleton of diabetic rats with type-2 diabetes and neuropathy is characterized by regional changes of size, form, mineral content and density and concomitantly with regional abnormalities of the IGF- system and neuropeptides suggesting that also local factors beyond systemic play an important role in the development of diabetic osteopathy.
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| 3. |
- Ahmad, T., et al.
(author)
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Frequency and outcomes of undiagnosed diabetes mellitus in patients presenting with acute myocardial infarction
- 2020
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In: Medical Forum Monthly. - : Medical Forum Monthly. - 1029-385X. ; 31:12, s. 3-7
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Journal article (peer-reviewed)abstract
- Objective: To find out frequency and outcomes of undiagnosed diabetes mellitus in patients presenting with acute ST elevation myocardial infarction (STEMI). Study Design: Descriptive / Cross-Sectional Study Place and Duration of study: This study was conducted at the Cardiology Department, Lady Reading Hospital, Peshawar from November 2018 to May 2019. Materials and Methods: Patient of either gender having age ranging between 30-75 years old with acute STEMI who present within 12 hours of symptoms and with no past history of documented diabetes mellitus were included in the study. Venous blood samples for laboratory data, including random blood sugar, two fasting blood sugar and HBA1c using hitachi modular evo p800 machine was done. Results: A total of 158 patients having acute STEMI were studied. Males were 68.4% (n=108).The mean age was 59.65 ±10.80 years. Frequency of undiagnosed diabetes mellitus was 31.64 % (n = 50). In non-diabetics stress hyperglycemia was found in 51.85 % (n=56) patients. Among various types of STEMI, anterior STEMI was more common presentation 34.1 % (n=54. p= 0.85). Mean HBA1C was 6.19 ± 1.87%. Frequency of Ventricular tachycardia (VT) was 22.2 % in which undiagnosed diabetics were n=18 (p=0.004).Ventricular fibrillation was present in 13.3 % patients with undiagnosed diabetics were n=14 (p=0.001). Frequency of AF was 13.9% (n=22) with undiagnosed diabetics having AF in n=13 (p=0.003). SVT was present in 5.7% (n=9) patients with not significant difference between two groups (p=0.017). Among various mechanical complications VSR was present in 10 % (n=16) of patients (p=0.001), cardiogenic shock in 11.1 % (n=18) patients (p=0.004), acute LVF was present in 15.8 % patients (p=0.017). Conclusion: In our study we concluded that one third of patients having acute ST elevation myocardial infarction have undiagnosed diabetes mellitus (31.64 %, n = 50). The most common complication was ventricular tachycardia among electrical complication and LVF among mechanical complication.
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| 4. |
- Ahmad, Tauseef, 1986, et al.
(author)
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Methodology for Power-Aware Coherent Receiver Design
- 2013
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In: Optics InfoBase Conference Papers. - 2162-2701. ; , s. SPT4D.4-
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Conference paper (peer-reviewed)abstract
- We describe a methodology to design and evaluate DSP hardware for a coherent receiver. Important parameters that can be assessed include DSP power consumption and chip area.
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- Goodfellow, Bradley W., 1971-
(author)
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Relict non-glacial surfaces and autochthonous blockfields in the northern Swedish mountains
- 2008
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Doctoral thesis (other academic/artistic)abstract
- Relict non-glacial surfaces occur in many formerly glaciated landscapes, where they represent areas that have escaped significant glacial modification. Frequently distinguished by blockfield mantles, relict non-glacial surfaces are important archives of long-term weathering and landscape evolution processes. The aim of this thesis is to examine the distribution, weathering, ages, and formation of relict non-glacial surfaces in the northern Swedish mountains. Mapping of surfaces from aerial photographs and analysis in a GIS revealed five types of relict non-glacial surfaces that reflect differences in surface process types or rates according to elevation, gradient, and bedrock lithology. Clast characteristics and fine matrix granulometry, chemistry, and mineralogy reveal minimal chemical weathering of the blockfields. Terrestrial cosmogenic nuclides were measured in quartz samples from two blockfield-mantled summits and a numerical ice sheet model was applied to account for periods of surface burial beneath ice sheets and nuclide production rate changes attributable to glacial isostasy. Total surface histories for each summit are almost certainly, but not unequivocally, confined to the Quaternary. Maximum modelled erosion rates are as low as 4.0 mm/kyr, which is likely to be near the low extreme for relict non-glacial surfaces in this landscape. The blockfields of the northern Swedish mountains are Quaternary features formed through subsurface physical weathering processes. While there is no need to appeal to Neogene chemical weathering to explain blockfield origins, these surfaces have remained continuously regolith-mantled and non-glacial since their inception. Polygenetic surface histories are therefore indicated, where the large-scale surface morphologies are potentially older than their regolith mantles.
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| 8. |
- Rawcliffe, Denise F. R., 1988-
(author)
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The regulation of incorrect splicing of ISCU in hereditary myopathy with lactic acidosis
- 2018
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Doctoral thesis (other academic/artistic)abstract
- Patients suffering from hereditary myopathy with lactic acidosis (HML) can be found in the northern Swedish counties of Ångermanland and Västerbotten. HML is a rare autosomal recessive disease where patients display a low tolerance to exercise at an early age. Exercise can trigger symptoms such as palpitations, tachycardia, muscle cramps and dyspnoea. Extensive exercise or strict diets can result in myoglobinuria and life-threatening levels of lactic acid. The disease is caused by a nonsense G > C mutation (c.418 + 328G < C) in the last intron of the iron-sulphur (FeS) cluster assembly gene (ISCU), resulting in nonsense-mediated decay (NMD) of the transcript due to incorrect splicing. The ISCU protein is involved in the assembly of FeS clusters, which are essential cofactors for a wide range of proteins. Patient muscles display decreased levels of several FeS cluster proteins: mitochondrial aconitase in the tricarboxylic acid (TCA) cycle and Complex I, II (succinate dehydrogenase [SDH]) and III in the electron transport chain (ETC). The incorrect splicing of ISCU occurs to the highest extent in HML patient skeletal muscle, restricting the loss of ISCU protein to muscles, thereby preventing a more severe phenotype.We found that the incorrect splicing occurs to the highest extent in slow-fibre muscle, which may be caused by the serine/arginine-rich splicing factor (SRSF3) as it is expressed at higher levels in slow-fibre muscle compared to other muscles, and since it is able to activate the incorrect splicing of ISCU. Following muscle, there is a gradual decrease of the incorrect splicing in heart, brain, liver and kidney, which is negatively correlated with the levels of the splicing inhibitor polypyrimidine-tract binding protein 1 (PTBP1). Overexpression of PTBP1 in HML patient myoblasts resulted in a drastic decrease in the incorrect splicing, while a PTBP1 knockdown had the opposite effect. Our results suggest that PTBP1 acts as a dominant inhibitor of the incorrect splicing and is likely the main cause for the tissue-specific splicing of ISCU in HML. We also identified RBM39 and MBNL1 as activators of the incorrect splicing of ISCU, which, together with the low levels of PTBP1, could explain the high levels of incorrect splicing in muscle.Since almost 95% of all human gene transcripts are alternatively spliced, it is not surprising that a wide range of diseases are caused by mutations that affect splicing. Further knowledge of the function of splicing, such as tissue-specific splicing, can provide vital information for the development of therapies for diseases caused by splicing.
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| 10. |
- Schwartz, Birgitta, et al.
(author)
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Conclusions
- 2012
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In: Societal Entrepreneurship. - Cheltenham : Edward Elgar Publishing. - 9781781006320 - 9781781006337 ; , s. 259-277
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Book chapter (peer-reviewed)
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