Diabetes mellitus and vascular lesions.

Cardiovascular complications represent by far the most severe manifestations of diabetes mellitus. Treatment aimed at stopping progression of vascular lesions may fall short if initiated when the disease becomes clinically evident. Therefore, identification of the earliest vascular disfunctions may offer the best opportunity to interfere with pathogenic mechanisms and avoid progression of diabetic vasculopathy. In this report, we present a few mechanisms that alter hemodynamic and metabolic homeostasis in the course of diabetes mellitus. Endothelial function with special emphasis on nitric oxide and oxidative stress, advanced glycation end products, and the renin angiotensin system are briefly discussed. New pharmacological agents that may favorably influence these parameters are presently undergoing clinical trials. However, tight control of plasma glucose and cardiovascular risk factors represent the cornerstone of the treatment in diabetes to slow progression of vascular disease.

Audit report on the North Iowa Juvenile Detention Services Commission for the year ended June 30, 2011

Audit report on the North Iowa Juvenile Detention Services Commission for the year ended June 30, 2011

Cardiorenal end points in a trial of aliskiren for type 2 diabetes.

BACKGROUND: This study was undertaken to determine whether use of the direct renin inhibitor aliskiren would reduce cardiovascular and renal events in patients with type 2 diabetes and chronic kidney disease, cardiovascular disease, or both. METHODS: In a double-blind fashion, we randomly assigned 8561 patients to aliskiren (300 mg daily) or placebo as an adjunct to an angiotensin-converting-enzyme inhibitor or an angiotensin-receptor blocker. The primary end point was a composite of the time to cardiovascular death or a first occurrence of cardiac arrest with resuscitation; nonfatal myocardial infarction; nonfatal stroke; unplanned hospitalization for heart failure; end-stage renal disease, death attributable to kidney failure, or the need for renal-replacement therapy with no dialysis or transplantation available or initiated; or doubling of the baseline serum creatinine level. RESULTS: The trial was stopped prematurely after the second interim efficacy analysis. After a median follow-up of 32.9 months, the primary end point had occurred in 783 patients (18.3%) assigned to aliskiren as compared with 732 (17.1%) assigned to placebo (hazard ratio, 1.08; 95% confidence interval [CI], 0.98 to 1.20; P=0.12). Effects on secondary renal end points were similar. Systolic and diastolic blood pressures were lower with aliskiren (between-group differences, 1.3 and 0.6 mm Hg, respectively) and the mean reduction in the urinary albumin-to-creatinine ratio was greater (between-group difference, 14 percentage points; 95% CI, 11 to 17). The proportion of patients with hyperkalemia (serum potassium level, ≥6 mmol per liter) was significantly higher in the aliskiren group than in the placebo group (11.2% vs. 7.2%), as was the proportion with reported hypotension (12.1% vs. 8.3%) (P<0.001 for both comparisons). CONCLUSIONS: The addition of aliskiren to standard therapy with renin-angiotensin system blockade in patients with type 2 diabetes who are at high risk for cardiovascular and renal events is not supported by these data and may even be harmful. (Funded by Novartis; ALTITUDE ClinicalTrials.gov number, NCT00549757.).

Is there histomorphological evidence of plantar metatarsal fat pad atrophy in patients with diabetes?

The etiology of diabetic foot ulceration remains incompletely understood. Among other factors such as foot deformity in the presence of neuropathy, plantar fat pad atrophy has been identified as a contributory factor in diabetic foot ulceration. An association between fat pad atrophy and diabetic foot ulceration has been documented by imaging and histomorphological analysis of the calcaneal fat pad. However, histomorphological analysis of the metatarsal fat pad has not been performed to date. The present study entailed 14 patients with diabetes and 14 nondiabetic controls and was aimed at documenting histomorphological evidence for presumed plantar metatarsal fat pad atrophy in patients with diabetes. Histological stains and computer-assisted planimetry were performed on samples of metatarsal fat obtained during forefoot surgery. The histomorphological and planimetric analyses of adipocyte cross-sectional area and nuclear density demonstrated no differences between patients with diabetes and control patients. Our findings demonstrate that systemic atrophy of the metatarsal fat pad is not present in the diabetic foot and may not explain the structural changes previously proposed by noninvasive imaging. Level of Clinical Evidence: 3.

Cerebral infarction in diabetes: Clinical pattern, stroke subtypes,and predictors of in-hospital mortality

Background: To compare the characteristics and prognostic features of ischemic stroke in patients with diabetes and without diabetes, and to determine the independent predictors of in-hospital mortality in people with diabetes and ischemic stroke.Methods: Diabetes was diagnosed in 393 (21.3%) of 1,840 consecutive patients with cerebral infarction included in a prospective stroke registry over a 12-year period. Demographic characteristics, cardiovascular risk factors, clinical events, stroke subtypes, neuroimaging data, and outcome in ischemic stroke patients with and without diabetes were compared. Predictors of in-hospital mortality in diabetic patients with ischemic stroke were assessed by multivariate analysis. Results: People with diabetes compared to people without diabetes presented more frequently atherothrombotic stroke (41.2% vs 27%) and lacunar infarction (35.1% vs 23.9%) (P < 0.01). The in-hospital mortality in ischemic stroke patients with diabetes was 12.5% and 14.6% in those without (P = NS). Ischemic heart disease, hyperlipidemia, subacute onset, 85 years old or more, atherothrombotic and lacunar infarcts, and thalamic topography were independently associated with ischemic stroke in patients with diabetes, whereas predictors of in-hospital mortality included the patient's age, decreased consciousness, chronic nephropathy, congestive heart failure and atrial fibrillation. Conclusion: Ischemic stroke in people with diabetes showed a different clinical pattern from those without diabetes, with atherothrombotic stroke and lacunar infarcts being more frequent. Clinical factors indicative of the severity of ischemic stroke available at onset have a predominant influence upon in-hospital mortality and may help clinicians to assess prognosis more accurately.

Gestational diabetes mellitus and the risk of metabolic syndrome: a population-based study in Lausanne, Switzerland.

AIMS: To investigate the relationships between gestational diabetes mellitus (GDM) and the metabolic syndrome (MS), as it was suggested that insulin resistance was the hallmark of both conditions. To analyse post-partum screening in order to identify risk factors for the subsequent development of type 2 diabetes mellitus (DM). METHODS: A retrospective analysis of all singleton pregnancies diagnosed with GDM at the Lausanne University Hospital for 3 consecutive years. Pre-pregnancy obesity, hypertension and dyslipidaemia were recorded as constituents of the MS. RESULTS: For 5788 deliveries, 159 women (2.7%) with GDM were identified. Constituents of the MS were present before GDM pregnancy in 26% (n = 37/144): 84% (n = 31/37) were obese, 38% (n = 14/37) had hypertension and 22% (n = 8/37) had dyslipidaemia. Gestational hypertension was associated with obesity (OR = 3.2, P = 0.02) and dyslipidaemia (OR = 5.4, P=0.002). Seventy-four women (47%) returned for post-partum OGTT, which was abnormal in 20 women (27%): 11% (n = 8) had type 2 diabetes and 16% (n = 12) had impaired glucose tolerance. Independent predictors of abnormal glucose tolerance in the post-partum were: having > 2 abnormal values on the diagnostic OGTT during pregnancy and presenting MS constituents (OR = 5.2, CI 1.8-23.2 and OR = 5.3, CI 1.3-22.2). CONCLUSIONS: In one fourth of GDM pregnancies, metabolic abnormalities precede the appearance of glucose intolerance. These women have a high risk of developing the MS and type 2 diabetes in later years. Where GDM screening is not universal, practitioners should be aware of those metabolic risks in every pregnant woman presenting with obesity, hypertension or dyslipidaemia, in order to achieve better diagnosis and especially better post-partum follow-up and treatment.

Criminal and Juvenile Justice Planning Advisory Council Progress on the Long-range Justice System Plan, January 2010

Iowa Code Section 216A.135 requires the Criminal and Juvenile Justice Planning Advisory Council (CJJPAC) to submit a long-range plan for Iowa's justice system to the Governor and General Assembly every five years. The Criminal and Juvenile Justice Advisory Council directed that the 2005 plan be developed with input from the public. A public hearing was held in September 2004, utilizing the Iowa Communications Network at five sites across Iowa. Using the information gained, the Council developed new goals and strategies and modified others from the 2000 plan. The 2005 Long Range Goals for Iowa’s Criminal and Juvenile Justice Systems, organized as follows, are meant to facilitate analyses and directions for justice system issues and concerns in Iowa.

Iowa Criminal and Juvenile Justice Plan, 1998

Pursuant to Iowa Code 216A, subchapter 9, CJJP is required to issue an annual report containing long-range systems goals, special issue planning recommendations and research findings. CJJP’s 1998 response to its reporting requirement is replicated in the manner of the distribution of the 1997 Update. Again this year, CJJP is issuing one large document which contains many separate reports. Single-issue 1998 Update reports will be made available based on reader interest and need. Having utilized this disseminating approach of CJJP research and reports in 1997, it proved to be cost effective and responsive to the planning activities and information needs of Iowa’s policy makers, justice system officials and others.

Role of the JNK-interacting protein 1/islet brain 1 in cell degeneration in Alzheimer disease and diabetes.

Numerous epidemiological studies and some pharmacological clinical trials show the close connection between Alzheimer disease (AD) and type 2 diabetes (T2D) and thereby, shed more light into the existence of possible similar pathogenic mechanisms between these two diseases. Diabetes increases the risk of developing AD and sensitizers of insulin currently used as diabetes drugs can efficiently slow cognitive decline of the neurological disorder. Deposits of amyloid aggregate and hyperphosphorylation of tau, which are hallmarks of AD, have been also found in degenerating pancreatic islets beta-cells of patients with T2D. These events may have a causal role in the pathogenesis of the two diseases. Increased c-Jun NH(2)-terminal kinase (JNK) activity is found in neurofibrillary tangles (NFT) of AD and promotes programmed cell death of beta-cells exposed to a diabetic environment. The JNK-interacting protein 1 (JIP-1), also called islet brain 1 (IB1) because it is mostly expressed in the brain and islets, is a key regulator of the JNK pathway in neuronal and beta-cells. JNK, hyperphosphorylated tau and IB1/JIP-1 all co-localize with amyloids deposits in NFT and islets of AD and patients with T2D. This review discusses the role of the IB1/JIP-1 and the JNK pathway in the molecular pathogenesis of AD and T2D.

Dusproportionate Minority Contact in Iowa's Juvenile Justice System, April 2006

This report was developed to provide summary information to allow state agency staff, practitioners and juvenile justice system officials to access a specific section of Iowa’s Three Year Plan. It includes the Disproportionate Minority Contact (DMC) section of Iowa’s 2006 Juvenile Justice and Delinquency Prevention Act formula grant Three-Year Plan. The complete Three Year Plan serves as Iowa’s application for Juvenile Justice and Delinquency Prevention Act formula grant funding.

Iowa Criminal and Juvenile Justice Plan, 2006 Update

This report discusses a number of topics and presents data and other information in response to Iowa Code Section 216A.135’s mandate for an annual Plan Update. It was prepared as an edocument and relies mainly on links to other documents which, when combined, make up the complete report. The outline that follows names the issues being presented this year by the CJJPAC and is both a table of contents and a “site-map” for the report.

2007 State of Iowa Juvenile Justice and Delinquency Prevention Act Formule Grand Update

This document is Iowa’s 2007 JJDP Act formula grant three year plan update. When specific items of this plan are unchanged from the previously submitted 2006 plan, we have reflected accordingly in the respective topic areas of this document. The bulk of this 2007 plan is an “update” of the program plan completed since submission of the original 2006 plan. The Division of Criminal and Juvenile Justice Planning (CJJP) wrote Iowa’s three year plan update. CJJP is the state agency responsible for administering the JJDP Act in Iowa. Federal officials refer to state administering agencies as the state planning agency (SPA). The Plan was developed and approved by Iowa’s Juvenile Justice Advisory Council. That Council assists with administration of the JJDP Act, and also provides guidance and direction to the SPA, the Governor and the legislature regarding juvenile justice issues in Iowa. Federal officials refer to such state level groups as state advisory groups (SAG’s).

2006-2007 Academic Year Juvenile Court Schoolbased Liaison Statewide Data

Prepared by the Division of Criminal and Juvenile Justice Planning, Iowa Department of Human Rights