A-1 - Monthly Public Assistance Statistical Report Family Investment Program, July 2010

A-1 - Monthly Public Assistance Statistical Report Family Investment Program

A-1 - Monthly Public Assistance Statistical Report Family Investment Program, August 2010

A-1 - Monthly Public Assistance Statistical Report Family Investment Program

Rôle du médecin interniste ou du généraliste dans le diagnostic et le suivi d'une collagénose [Family physician and connective tissue disorders].

The exact place of the family physician in the diagnosis and management of connective tissue disease is poorly studied moreover will essentially depend on the health system and the organization of medical network of each country. Connective tissue diseases are rare and complex diseases that require in all cases referral to specialists for their diagnosis as well as monitoring. All patients must still keep a family doctor whose importance increases more and more as our specialized treatments prolong survival of patients who become chronically ill with multi-organic sequelae. A closely interaction between the various specialists and family physicians is necessary to ensure a good long-term follow-up.

A-1 - Monthly Public Assistance Statistical Report Family Investment Program, September 2010

A-1 - Monthly Public Assistance Statistical Report Family Investment Program

Mothers' and fathers' views of the interdependence of their relationships with their infant: a systems perspective on early family relationships.

This study examined the interrelatedness of mother-infant and father-infant relationships as they develop over the first 4 months postpartum as well as the dynamics used by the couple to balance these relationships. First-time mother-father couples (n = 18) were interviewed separately at 1, 6, and 16 weeks postpartum using the Parent-Infant Relationship Interview. The data were analyzed using in-depth qualitative strategies. The parents' core themes of their early family relationships ranged from an undifferentiated unit at 1 week, to being a highly disorganized unit at 6 weeks, to a more integrated unit at 16 weeks. These results suggest that one should be thinking of early family relationships and parenting in terms of "messy processes" out of which new ways of being together are created. This disorganization plays a fundamental role in the establishment of early family relationships and warrants further empirical and clinical attention.

A-1 - Monthly Public Assistance Statistical Report Family Investment Program, October2010

A-1 - Monthly Public Assistance Statistical Report Family Investment Program

A-1 - Monthly Public Assistance Statistical Report Family Investment Program, November 2010

A-1 - Monthly Public Assistance Statistical Report Family Investment Program

New Findings in a Global Approach to Dissect the Whole Phenotype of PLA2G6 Gene Mutations.

Mutations in PLA2G6 gene have variable phenotypic outcome including infantile neuroaxonal dystrophy, atypical neuroaxonal dystrophy, idiopathic neurodegeneration with brain iron accumulation and Karak syndrome. The cause of this phenotypic variation is so far unknown which impairs both genetic diagnosis and appropriate family counseling. We report detailed clinical, electrophysiological, neuroimaging, histologic, biochemical and genetic characterization of 11 patients, from 6 consanguineous families, who were followed for a period of up to 17 years. Cerebellar atrophy was constant and the earliest feature of the disease preceding brain iron accumulation, leading to the provisional diagnosis of a recessive progressive ataxia in these patients. Ultrastructural characterization of patients' muscle biopsies revealed focal accumulation of granular and membranous material possibly resulting from defective membrane homeostasis caused by disrupted PLA2G6 function. Enzyme studies in one of these muscle biopsies provided evidence for a relatively low mitochondrial content, which is compatible with the structural mitochondrial alterations seen by electron microscopy. Genetic characterization of 11 patients led to the identification of six underlying PLA2G6 gene mutations, five of which are novel. Importantly, by combining clinical and genetic data we have observed that while the phenotype of neurodegeneration associated with PLA2G6 mutations is variable in this cohort of patients belonging to the same ethnic background, it is partially influenced by the genotype, considering the age at onset and the functional disability criteria. Molecular testing for PLA2G6 mutations is, therefore, indicated in childhood-onset ataxia syndromes, if neuroimaging shows cerebellar atrophy with or without evidence of iron accumulation.

Mitochondrial Fatty Acid Oxidation in Obesity

Significance: Current lifestyles with high-energy diets and little exercise are triggering an alarming growth in obesity. Excess of adiposity is leading to severe increases in associated pathologies, such as insulin resistance, type 2 diabetes, atherosclerosis, cancer, arthritis, asthma, and hypertension. This, together with the lack of efficient obesity drugs, is the driving force behind much research. Recent Advances: Traditional anti-obesity strategies focused on reducing food intake and increasing physical activity. However, recent results suggest that enhancing cellular energy expenditure may be an attractive alternative therapy. Critical Issues: This review evaluates recent discoveries regarding mitochondrial fatty acid oxidation (FAO) and its potential as a therapy for obesity. We focus on the still controversial beneficial effects of increased FAO in liver and muscle, recent studies on how to potentiate adipose tissue energy expenditure, and the different hypotheses involving FAO and the reactive oxygen species production in the hypothalamic control of food intake. Future Directions: The present review aims to provide an overview of novel anti-obesity strategies that target mitochondrial FAO and that will definitively be of high interest in the future research to fight against obesity-related disorders. Antioxid. Redox Signal. 00, 000000.

Bistability of mitochondrial respiration underlies paradoxical reactive oxygen species generation induced by anoxia

Increased production of reactive oxygen species (ROS) in mitochondria underlies major systemic diseases, and this clinical problem stimulates a great scientific interest in the mechanism of ROS generation. However, the mechanism of hypoxia-induced change in ROS production is not fully understood. To mathematically analyze this mechanism in details, taking into consideration all the possible redox states formed in the process of electron transport, even for respiratory complex III, a system of hundreds of differential equations must be constructed. Aimed to facilitate such tasks, we developed a new methodology of modeling, which resides in the automated construction of large sets of differential equations. The detailed modeling of electron transport in mitochondria allowed for the identification of two steady state modes of operation (bistability) of respiratory complex III at the same microenvironmental conditions. Various perturbations could induce the transition of respiratory chain from one steady state to another. While normally complex III is in a low ROS producing mode, temporal anoxia could switch it to a high ROS producing state, which persists after the return to normal oxygen supply. This prediction, which we qualitatively validated experimentally, explains the mechanism of anoxia-induced cell damage. Recognition of bistability of complex III operation may enable novel therapeutic strategies for oxidative stress and our method of modeling could be widely used in systems biology studies.

Audit report on the Iowa Federal Family Education Loan Program Division, a Division of the Iowa College Student Aid Commission, for the year ended June 30, 2010

Audit report on the Iowa Federal Family Education Loan Program Division, a Division of the Iowa College Student Aid Commission, for the year ended June 30, 2010

Achondrogenesis Type 1B.

DISEASE CHARACTERISTICS: Clinical features of achondrogenesis type 1B (ACG1B) include extremely short limbs with short fingers and toes, hypoplasia of the thorax, protuberant abdomen, and hydropic fetal appearance caused by the abundance of soft tissue relative to the short skeleton. The face is flat, the neck is short, and the soft tissue of the neck may be thickened. Death occurs prenatally or shortly after birth. DIAGNOSIS/TESTING: The diagnosis of ACG1B rests on a combination of clinical, radiologic, and histopathologic features. SLC26A2 (DTDST) is the only gene known to be associated with ACG1B. Molecular genetic testing is available on a clinical basis. MANAGEMENT: Treatment of manifestations: palliative care for liveborn neonates. GENETIC COUNSELING: ACG1B is inherited in an autosomal recessive manner. At conception, each sib of a proband with ACG1B has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Once an at-risk sib is known to be unaffected, the risk of his/her being a carrier is 2/3. Carrier testing for at-risk relatives and prenatal testing for pregnancies at increased risk are possible if both disease-causing alleles in the family are known and the carrier status of the parents has been confirmed. Ultrasound examination after 14-15 weeks' gestation can be diagnostic.

A-1 - Monthly Public Assistance Statistical Report Family Investment Program, December 2010

A-1 - Monthly Public Assistance Statistical Report Family Investment Program

Regulation of lymphocyte proliferation and death by FLIP.

Lymphocyte homeostasis is a balance between lymphocyte proliferation and lymphocyte death. Tight control of apoptosis is essential for immune function, because its altered regulation can result in cancer and autoimmunity. Signals from members of the tumour-necrosis-factor receptor (TNF-R) family, such as Fas and TNF-R1, activate the caspase cascade and result in lymphocyte death by apoptosis. Anti-apoptotic proteins, such as FLIP (also known as FLICE/caspase-8 inhibitory protein) have recently been identified. FLIP expression is tightly regulated in T cells and might be involved in the control of both T-cell activation and death. Abnormal expression of FLIP might have a role not only in autoimmune diseases, but also in tumour development and cardiovascular disorders.