Implementing QR Code Technology in Medical Device Pacakage

The medical device industry strives to improve the delivery of key device information through the package to patients, doctors and end users. To achieve this goal Indications For Use (IFU) and user manuals have been major tools and are necessary components required in Medical Device Package according to Food and Drug Administration (FDA) standards. Historically there have been challenges caused by packaging information materials aspects such as manufacturing, transportation and translation. The need for extensive packaging and labelling has ultimately contributed to increased cost of manufacturing for devices. It is also important to know what information a customer needs and recognize that the safety of the consumer is of the utmost importance. The development and implementation of new technologies and procedures in a medical device industry may be complicated and slow but it is a necessity to improve safety and provide maximum comfort to the end user. Barcodes and Two Dimensional code have been used in the medical device industry for tracking purposes; however, the focus of this thesis was using QR codes (two-Dimensional barcode) in medical device package without IFU, user guides and manuals to enhance patient safety, reduce cost and enhance the breadth of information available to the ultimate users. Access to the information was achieved by just taking a picture or scanning the QR code which was printed on a medical device package. This thesis also assesses the feasibility of implementing the QR code technology on medical device package and a case study is conducted that elaborates on the cost analysis

Cost and Consequences of Sedentary Living: New Battleground for an Old Enemy

The purpose of this review is to update our earlier review by itemizing, as best we can, the costs and consequences of sedentary living, and thus provide cost reasons to fight a war against sedentary lifestyles

Brain fatty acid synthase activates PPARa to maintain energy homeostasis

Central nervous system control of energy balance affects susceptibility to obesity and diabetes, but how fatty acids, malonyl-CoA, and other metabolites act at this site to alter metabolism is poorly understood. Pharmacological inhibition of fatty acid synthase (FAS), rate limiting for de novo lipogenesis, decreases appetite independently of leptin but also promotes weight loss through activities unrelated to FAS inhibition. Here we report that the conditional genetic inactivation of FAS in pancreatic β cells and hypothalamus produced lean, hypophagic mice with increased physical activity and impaired hypothalamic PPARα signaling. Administration of a PPARα agonist into the hypothalamus increased PPARα target genes and normalized food intake. Inactivation of β cell FAS enzyme activity had no effect on islet function in culture or in vivo. These results suggest a critical role for brain FAS in the regulation of not only feeding, but also physical activity, effects that appear to be mediated through the provision of ligands generated by FAS to PPARα. Thus, 2 diametrically opposed proteins, FAS (induced by feeding) and PPARα (induced by starvation), unexpectedly form an integrative sensory module in the central nervous system to orchestrate energy balance

Metabolic improvements following Roux-en-Y surgery assessed by solid meal test in subjects with short duration type 2 diabetes

BACKGROUND: Glucose homeostasis improves within days following Roux-en-Y gastric bypass (RYGB) surgery. The dynamic metabolic response to caloric intake following RYGB has been assessed using liquid mixed meal tolerance tests (MMTT). Few studies have evaluated the glycemic and hormonal response to a solid mixed meal in subjects with diabetes prior to, and within the first month following RYGB. METHODS: Seventeen women with type 2 diabetes of less than 5 years duration participated. Fasting measures of glucose homeostasis, lipids and gut hormones were obtained pre- and post-surgery. MMTT utilizing a solid 4 oz chocolate pudding performed pre-, 2 and 4 weeks post-surgery. Metabolic response to 4 and 2 oz MMTT assessed in five diabetic subjects not undergoing surgery. RESULTS: Significant reductions in fasting glucose and insulin at 3 days, and in fasting betatrophin, triglycerides and total cholesterol at 2 weeks post-surgery. Hepatic insulin clearance was greater at 3 days post-surgery. Subjects exhibited less hunger and greater feelings of fullness and satisfaction during the MMTT while consuming 52.9 ± 6.5% and 51.0 ± 6.5% of the meal at 2 and 4 weeks post-surgery respectively. At 2 weeks post-surgery, glucose and insulin response to MMTT were improved, with greater GLP-1 and PYY secretion. Improved response to solid MMTT not replicated by consumption of smaller pudding volume in diabetic non-surgical subjects. CONCLUSIONS: With a test meal of size and composition representative of the routine diet of post-RYGB subjects, improved glycemic and gut hormone responses occur which cannot be replicated by reducing the size of the MMTT in diabetic subjects not undergoing surgery

Topographical expression of class IA and class II phosphoinositide 3-kinase enzymes in normal human tissues is consistent with a role in differentiation

BACKGROUND: Growth factor, cytokine and chemokine-induced activation of PI3K enzymes constitutes the start of a complex signalling cascade, which ultimately mediates cellular activities such as proliferation, differentiation, chemotaxis, survival, trafficking, and glucose homeostasis. The PI3K enzyme family is divided into 3 classes; class I (subdivided into IA and IB), class II (PI3K-C2α, PI3K-C2β and PI3K-C2γ) and class III PI3K. Expression of these enzymes in human tissue has not been clearly defined. METHODS: In this study, we analysed the immunohistochemical topographical expression profile of class IA (anti-p85 adaptor) and class II PI3K (PI3K-C2α and PI3K-C2β) enzymes in 104 formalin-fixed, paraffin embedded normal adult human (age 33–71 years, median 44 years) tissue specimens including those from the gastrointestinal, genitourinary, hepatobiliary, endocrine, integument and lymphoid systems. Antibody specificity was verified by Western blotting of cell lysates and peptide blocking studies. Immunohistochemistry intensity was scored from undetectable to strong. RESULTS: PI3K enzymes were expressed in selected cell populations of epithelial or mesenchymal origin. Columnar epithelium and transitional epithelia were reactive but mucous secreting and stratified squamous epithelia were not. Mesenchymal elements (smooth muscle and endothelial cells) and glomerular epithelium were only expressed PI3K-C2α while ganglion cells expressed p85 and PI3K-C2β. All three enzymes were detected in macrophages, which served as an internal positive control. None of the three PI3K isozymes was detected in the stem cell/progenitor compartments or in B lymphocyte aggregates. CONCLUSIONS: Taken together, these data suggest that PI3K enzyme distribution is not ubiquitous but expressed selectively in fully differentiated, non-proliferating cells. Identification of the normal in vivo expression pattern of class IA and class II PI3K paves the way for further analyses which will clarify the role played by these enzymes in inflammatory, neoplastic and other human disease conditions

Role of Protein Prenylation in Cellular Proliferation

Prenylation is a post-translational, covalent modification of a protein by the attachment of a lipophilic isoprenoid group, linked by a thioether bond to a cysteine at or near to the carboxyl terminus of the protein. Ras is one of the important proteins which undergoes such modification at the C-terminus CAAX box motif (where C=Cys, A=aliphatic amino acid, X=usually Ser or Met) by a 15C isoprenoid moiety, farnesyl, and is mediated by the enzyme, farnesyltransferase. Oncogenic forms of Ras have been shown to lose their transforming activity when farnesylation is prevent. Given that Ras proteins are implicated in a majority of human pancreatic and colorectal cancers, blocking Ras farnesylation would be a good strategy for developing new anti- cancer treatments. Benzodiazepine peptidomimetics, which mimic a natural dipeptide turn of the two aliphatic residues of the CAAX box, are effective inhibitors of farnesyltransferase, and normalizes the morphology of Rat1 cells transformed with H-ras (v12). The purpose of this study was to further characterize the potency, toxicity, and cellular uptake of the various benzodiazepine analogs using the Met18b-2 cell line as a model. Another aspect of the study was to investigate the reversion of compactin-induced cell rounding with prenyl alcohols. Since compactin-induced cell rounding was known to be reversed by mevalonate, the possibility of such reversion was investigated with prenyl alcohols to demonstrate that the control of cell shape is mediated by nonsterol products of the mevalonate pathway, and in turn demonstrate a salvage pathway for the prenyl alcohols. The results provide preliminary evidence for a salvage pathway, where the alcohols recycle back to the mono-and di-phosphates. The activity of the prenyl kinases, which phosphorylate the corresponding prenyl alcohols to the phosphates were also assayed. Consequently, these data support the possibility of the control of cellular growth and cell shape maintenance by prenylated proteins

Modulation of replicative senescence of skeletal muscle satellite cells by insulin -like growth factor-I (IGF-I)

Growth and regeneration of postnatal skeletal muscle requires a population of mononuclear myogenic cells, called satellite cells to add/replace myonuclei, which are postmitotic. Wedged between the sarcolemma and the basal lamina of the skeletal muscle fiber, these cells function as the stem cells of mature muscle fibers. Like other normal diploid cells, satellite cells undergo cellular senescence. Investigations of aging in both rodents and humans have shown that satellite cell self-renewal capacity decreases with advanced age. As a consequence, this could be a potential reason for the characteristically observed age-associated loss in skeletal muscle mass (sarcopenia). This provided the rationale that any intervention that can further increase the proliferative capacity of these cells should potentially be able to either delay, or even prevent sarcopenia. Using clonogenicity assays to determine a cell\u27s proliferation potential, these studies have shown that IGF-I enhances the doubling potential of satellite cells from aged rodents. Using a transgenic model, where the mice express the IGF-I transgene specifically in their striated muscles, some of the underlying biochemical mechanisms for the observed increase in replicative life span were delineated. These studies have revealed that IGF-I activates the PI3/Akt pathway to mediate downregulation of p27KIP1, which consequently is associated with an increase in cyclin E-cdk2 kinase activity, phosphorylation of pRb, and upregulation of cyclin A protein. However, the beneficial effects of IGF-I on satellite cell proliferative potential appears to be limited as chronic overexpression of IGF-I in skeletal muscles did not protect against sarcopenia in 18-mo old mice, and was associated with an exhaustion of satellite cell replicative reserves. These results have shown that replicative senescence can be modulated by environmental factors using skeletal muscle satellite cells as a model system. A better understanding of the molecular basis for enhancement of proliferative capacity by IGF-I will provide a rational basis for developing more effective counter-measures against physical frailty. However, the implications of these studies are that these beneficial effects of enhanced proliferative potential by IGF-I may only be over a short-term period, and other alternative approaches may need to be considered