Type I diabetics

Ling Zhi-8 (LZ-8) is an immunomodulatory protein (29,30) isolated from the mycelial extract of Ganoderma lucidium, that has been purified and shown to stimulate mouse spleen and human peripheral blood lymphocytes. LZ-8 is able to inhibit antibody production and prevent the development of autoimmune type I diabetes in NOD mice. 

On the other hand, EFN-a may also be involved in the activation of autoreactive T-cells as has been proposed for type I diabetes. An DFN-a inducible superantigen, encoded by the truncated envelope gene of a human endogenous retrovirus and specifically activating V 37 T-cells, has been detected in pancreatic lesions from type I diabetes patients, infiltrated by V 37 T-cells. Since IFN-a expression could be detected in pancreatic (3 cells in conceit with persistent viral infections, there is a clear link between viral infections and autoimmunity via IFN-a-stimulated superantigen expression. 

If the body is unable to neutralize acids due to a disease or other problem, a condition called acidosis can result. Acidosis occurs when the bloods pH goes below its normal level of 7.35. One disease that can cause acidosis is diabetes. Diabetic acidosis is caused by a lack of insulin. This condition most often occurs when a Type I diabetic misses his or her scheduled dose of insulin. 

Wilson SB et al. Multiple differences in gene expression in regulatory V24JQ T cells from identical twins discordant for type I diabetes. Proc Natl Acad Sci USA 2000 97 7411-7416. 

A 30-year-old type I diabetic with renal complications develops acute pyelonephritis F aeruginosa is found in urine cultures and blood cultures. Combined therapy is instituted with an aminoglycoside and which of the following ... 

Delorme, D. and Miller, S.C., Dietary consumption of Echinacea by mice afflicted with autoimmune (type I) diabetes effect of consuming the herb on hemopoietic and immune cell dynamics, Autoimmunity, 38, 453, 2005. 

Raz, I., Eldor, R., and Naparstek, Y., Immune modulation for prevention of type I diabetes mellitus, Trends Biotechnol., 23, 128, 2005. 

Multiple sclerosis Lyme arthritis Type I diabetes Rheumatoid arthritis Lupus... 

Based on the information in the passage, which of the following best describes people with Type I diabetes ... 

Therapy for insulin-dependent diabetes mellitus is usually achieved by daily subcutaneous injections of insulin, and insulin-mimetics which can be orally administered may be useful for the treatment of type I diabetes (insulin dependent) if suitable complexes of low toxicity can be identified (510, 511). 

Children and patients suffering from IDDMI (type I diabetes) have increased Lp(a) levels that normalize under diabetic control of the disease (C13, Gl, L17, S2). Glycemic control in type II diabetes, in contrast, seems to have little effect on Lp(a) levels (H7). 

Salzer, B., Stavljenic, A., Jurgens, G., Dumic, M., and Radica, A., Polymorphism of apolipoprotein E, lipoprotein(a), and other lipoproteins in children with type I diabetes. Clin. Chem. (Winston-Salem, NC) 39, 1427-1432 (1993). 

Diabetes mellitus occurs when the human body does not produce enough insulin. This form of diabetes is called insulin-dependent diabetes mellitus (IDDM, or juvenile diabetes, or type I diabetes). IDDM is an autoimmune disease (see Exhibit 4.7) in which the j8 cells are targeted by the body s own immune system and progressively destroyed. Once destroyed, they are unable to produce insulin. 

Juvenile onset (type I) diabetes mellitus is caused by the destruction of insulin-producing B cells in the pancreas, necessitating replacement of insulin (daily dose approx. 40 U, equivalent to approx. 1.6 mg). 

Insulin, a pancreatic hormone, is a specific antidiabetic agent, especially for type I diabetes. Human insulin is a double-chain protein with molecular mass around 6000 that contains 51 amino acids (chain A—21 amino acids, chain B—30 amino acids), which are bound together by disulfide bridges. 

The pathogenesis of type I diabetes is autoimmune destruction of the cells of the pancreas. The factor or factors that trigger this autoimmune response are unknown. Predisposing factors appear to include certain major histocompatibility complex haplotypes and autoantibodies to various islet cell antigens. The progression of the autoimmune response is characterized by lymphocytic infiltration and destruction of the pancreatic cells resulting in insulin deficiency. Type I diabetes mellitus constitutes about 10% of cases of diabetes mellitus. 

Treating Diabetes Mellitus. There are two main types of diabetes. Type I diabetes (previously called insulin-dependent diabetes mellitus, IDDM) is a severe form which occurs most commonly in juveniles and young adults and which results from an absolute insulin deficiency arising from pancreatic B cell destruction, presumably via an immune-mediated mechanism. Type II diabetes (previously called non-insulin-dependent diabetes mellitus, NIDDM) is a milder, heterogeneous form of diabetes which occurs more... 

Insulin dependent or type I diabetes (IDDM). Formerly called juvenile onset, or ketone prone diabetes. It is an autoimmune disease of pancreatic (3-cells. Arises due to insulin insufficiency. 

Skyler, IS., W.T. Cefalu, I.A. Kourides, W.H. Landschulz, C.C. Balagtas, S.L. Cheng, and R.A. Gelfand, Efficacy of inhaled human insulin in type I diabetes mellitus a randomised proof-of-concept study. Lancet, 2001.357(9253) 331-5. 

Numerous studies have indicated that pro-inflammatory mediators (cytokines) are involved in the destruction of the insulin-producing p-cells of the pancreas in the development of type I diabetes. Tabatabaie et al. introduced cytokines and PBN into the pancreas of rats. The analysis of pancreatic extracts revealed that the cytokines stimulate the formation of lipid radicals. Radical generation did not occur in rats treated with streptozotocin, which destroys the P-cells.33 Evidence for the role of radicals in diabetes has also been provided by spin trapping studies in pancreatic homogenates, showing that streptozotocin, which is often used to induce the condition in laboratory animals, stimulates OH production.332 Other workers, using EPR to observe the decay of a spin probe in the abdomen of mice (at 1.2 GHz), have demonstrated that strep-... 

---