Evaluation of diabetic foot amputation rate

Acta Med Port. 2003 Nov-Dec;16(6):373-80. Epub 2003 Dec 1. [Evaluation of diabetic foot amputation rate]. [Article in Portuguese] Horta C, Vilaverde J, Mendes P, Gonçalves I, Serra L, Pinto PS, Almeida R, Carvalho R, Dores J, Serra MB. Serviços de Endocrinologia, Ortopedia e Cirurgia Vascular, Hospital Geral de Santo António, Porto. Abstract In 1987, it was created the first portuguese Diabetic Foot Clinic in Oporto, at the Hospital Geral de Santo António. The distinction between neuropathic and ischaemic foot was the key stone to reduce drastically the rate of major amputations in the first two years of activity. Since then and until 1995 the rate of major amputations had stabilised around 8%. The aim of the present study was to evaluate if there was any change in the last three years. A retrospective study was performed reviewing the clinical files of 843 new patients between 1998 and 2000. The 593 patients who presented with a foot ulcer with or without infection were selected: 60.4% with neuropathic foot and 39.6% with ischaemic one. Overall, 31 of the 593 patients with ulcer or infection were treated with major amputation (5.2%). There was a statistical difference between the major amputation outcome among the two types of foot (p < 0.001). Necrosis showed to carry a poor prognosis (30.7% in ischaemic foot vs 8,3% in neuropathic, p = 0.024). There was no further statistical significance for age, sex, type or duration of diabetes as risk factors for major amputation. This retrospective study has showed a slight reduction in the rate of major amputations since 1995. Poor prognosis was related to necrosis and ischaemic foot. Further improvement requires harder investment in patients' education, as well as in alerting the primary health care physicians, for the most unpredictable catastrophic complication of diabetes. PMID: 15631847 [PubMed - indexed for MEDLINE

BEZERRAS DE CORTE INFECTADAS NATURALMENTE COM PARASITAS GASTRINTESTINAIS EPIDEMIOLOGIA E TRATAMENTO SELETIVO

A severidade das infecções parasitárias depende em grande parte da quantidade e do tipo de parasita presente e do estado nutricional dos animais. O objetivo deste experimento foi associar o efeito da suplementação protéica e pastagem de alta qualidade com diferenças na resposta ao desafio parasitário em 36 novilhas de oito meses, naturalmente infectadas, durante 120 dias. Grupo I: pastagem (Avena strigosa e Lolium multiflorum); Grupo II: pastagem e níveis crescentes de suplemento (Triticum aestivum, farelo de trigo) de 0,3 a 1,5% do peso vivo (PV); Grupo III: pastagem e suplemento a 0,9% do PV e Grupo IV: pastagem e níveis decrescentes de suplemento. O grau de infecção parasitária foi determinado através da contagem de ovos por grama de fezes (OPG) e coprocultura. Animais com OPG acima de 600 foram tratados com levamisole (Ripercol®, Fort Dodge). A coprocultura revelou os gêneros Cooperia spp. e Trichostrongylus spp. O ganho de peso, o escore corporal e o nível parasitário foi semelhante entre os grupos. Foram administradas 24 doses de anti-helmíntico com baixo grau de repetibilidade dos animais. Determinou-se que o tratamento seletivo pode ser aplicado quando os animais dispõem de pastagem de alta qualidade e com baixo desafio parasitário, independente de suplementação alimentar. Naturally infected beef heifers with gastrintestinal parasites epidemiology and selective treatment Abstract The severity of parasite infections depends in part by the number and the parasite species as well as on the nutritional status of the host. The objective of this work was to determine the association between protein supplement and good quality pasture with parasite challenge infection in 36 naturally infected, 8 months old beef heifers during 120 days. Group I: pasture (Avena strigosa and Lolium multiflorum); Group II: pasture plus increasing levels of supplement (Triticum aestivum, wheat bran) from 0.3 to 1.5% of live weight (LW); Group III: pasture plus 0.9% LW of supplement; Group IV: pasture plus decreasing levels of supplement. Parasite infection was determined through fecal egg counts (EPG) and coproculture. All animals with EPG above 600 were treated with levamisole (Ripercol®, Fort Dodge). Coproculture displayed Cooperia sp. and Trichostrongylus sp. Weight gain, body condition score and parasite levels were similar among all groups. Twenty-four doses of the anthelmintic were administered with low animal repeatability. It was determined that the selective treatment may be used when animals have access to good quality pasture and a low parasite challenge, independently of the supplement offered

Information loss in local dissipation environments

The sensitivity of entanglement to the thermal and squeezed reservoirs' parameters is investigated regarding entanglement decay and what is called sudden-death of entanglement, ESD, for a system of two qubit pairs. The dynamics of information is investigated by means of the information disturbance and exchange information. We show that for squeezed reservoir, we can keep both of the entanglement and information survival for a long time. The sudden death of information is seen in the case of thermal reservoir

Decoherence in trapped ions due to polarization of the residual background gas

We investigate the mechanism of damping and heating of trapped ions associated with the polarization of the residual background gas induced by the oscillating ions themselves. Reasoning by analogy with the physics of surface electrons in liquid helium, we demonstrate that the decay of Rabi oscillations observed in experiments on 9Be+ can be attributed to the polarization phenomena investigated here. The measured sensitivity of the damping of Rabi oscillations with respect to the vibrational quantum number of a trapped ion is also predicted in our polarization model.Comment: 26 pdf pages with 5 figures, http://www.df.ufscar.br/~quantum

Dysfunction of the Heteromeric KV7.3/KV7.5 Potassium Channel is Associated with Autism Spectrum Disorders

Heterozygous mutations in the KCNQ3 gene on chromosome 8q24 encoding the voltage-gated potassium channel KV7.3 subunit have previously been associated with rolandic epilepsy and idiopathic generalized epilepsy (IGE) including benign neonatal convulsions. We identified a de novo t(3;8) (q21;q24) translocation truncating KCNQ3 in a boy with childhood autism. In addition, we identified a c.1720C > T [p.P574S] nucleotide change in three unrelated individuals with childhood autism and no history of convulsions. This nucleotide change was previously reported in patients with rolandic epilepsy or IGE and has now been annotated as a very rare SNP (rs74582884) in dbSNP. The p.P574S KV7.3 variant significantly reduced potassium current amplitude in Xenopus laevis oocytes when co-expressed with KV7.5 but not with KV7.2 or KV7.4. The nucleotide change did not affect trafficking of heteromeric mutant KV7.3/2, KV7.3/4, or KV7.3/5 channels in HEK 293 cells or primary rat hippocampal neurons. Our results suggest that dysfunction of the heteromeric KV7.3/5 channel is implicated in the pathogenesis of some forms of autism spectrum disorders, epilepsy, and possibly other psychiatric disorders and therefore, KCNQ3 and KCNQ5 are suggested as candidate genes for these disorders

Pre-B Cell Receptor Signaling Induces Immunoglobulin κ Locus Accessibility by Functional Redistribution of Enhancer-Mediated Chromatin Interactions

During B cell development, the precursor B cell receptor (pre-BCR) checkpoint is thought to increase immunoglobulin κ light chain (Igκ) locus accessibility to the V(D)J recombinase. Accordingly, pre-B cells lacking the pre-BCR signaling molecules Btk or Slp65 showed reduced germline Vκ transcription. To investigate whether pre-BCR signaling modulates Vκ accessibility through enhancer-mediated Igκ locus topology, we performed chromosome conformation capture and sequencing analyses. These revealed that already in pro-B cells the κ enhancers robustly interact with the ∼3.2 Mb Vκ region and its flanking sequences. Analyses in wild-type, Btk, and Slp65 single- and double-deficient pre-B cells demonstrated that pre-BCR signaling reduces interactions of both enhancers with Igκ locus flanking sequences and increases interactions of the 3′κ enhancer with Vκ genes. Remarkably, pre-BCR signaling does not significantly affect interactions between the intronic enhancer and Vκ genes, which are already robust in pro-B cells. Both enhancers interact most frequently with highly used Vκ genes, which are often marked by transcription factor E2a. We conclude that the κ enhancers interact with the Vκ region already in pro-B cells and that pre-BCR signaling induces accessibility through a functional redistribution of long-range chromatin interactions within the Vκ region, whereby the two enhancers play distinct roles

Micronuclei formation in liver fibrosis samples from patients infected by hepatitis C virus

Genetic research on fibrosis outset and its progression in chronic hepatitis (CH) by hepatitis C virus (HCV) are limited. The lack of cytogenetic data led us to investigate the presence of micronuclei (MNi), as a sign of genomic damage. Hepatocytes of hepatic parenchyma from 62 cases diagnosed with CH associated with HCV and displaying different degrees of fibrosis (F1-F4) were analyzed. These data were compared to 15 cases without fibrosis (F0). Twelve healthy liver parenchyma samples were included as control. All samples were obtained from paraffin-embedded archival material. Micronucleated hepatocytes (MN-Heps) were analyzed through Feulgen/Fast-green staining. Results showed that the rates of MN-Heps in the F4 group were statistically significant (p < 0.05) and higher than those in the control group. Like results were also obtained on comparing F4 with F0, F1, F2 and F3 cases. Conversely, differences were not significant (p > 0.05) on comparing F0, F1, F2, F3, one against the other, as well as individual versus control. Although chromosomal losses in CH were detected, it was shown that liver parenchyma with fibrosis in the initial stages (F1-F3) cannot be considered cytogenetically abnormal

Geographic Information Systems (GIS) in Assessing Dental Health

The present study investigated the distribution profile of dental caries and its association with areas of social deprivation at the individual and contextual level. The cluster sample consisted of 1,002 12-year-old schoolchildren from Piracicaba, SP, Brazil. The DMFT Index was used for dental caries and the Care Index was used to determine access to dental services. On the individual level, variables were associated with a better oral status. On the contextual level, areas were not associated with oral status. However, maps enabled determining that the central districts have better social and oral conditions than the deprived outlying districts

Polymorphism In Lep And Lepr May Modify Leptin Levels And Represent Risk Factors For Thyroid Cancer

Purpose. To understand the role of polymorphisms in the LEP (rs7799039 and rs2167270) and LEPR (rs1137101 and rs1137100) genes in DTC susceptibility and their effect on leptin levels. Methods. We studied 153 patients with DTC and 234 controls through TaqMan SNP Genotyping and ELISA, comparing these data to the clinicopathological data of patients with DTC. Results. Patients with AA genotype of rs7799039 had higher levels of serum leptin (9.22 ± 0.98 ng/mL) than those with AG genotype (10.07 ± 0.60 ng/mL; P = 0.005). Individuals with AG genotype of rs2167270 also produced higher serum leptin levels (10.05 ± 0.59 ng/mL) than the subjects with GG genotype (9.52 ± 0.79 ng/mL; P A) polymorphism and disease susceptibility and cardiovascular disease in patients with rheumatoid arthritis (2011) Clinical and Experimental Rheumatology, 29 (2), pp. 293-298Jiang, Y., Wilk, J.B., Borecki, I., Common variants in the 5' region of the leptin gene are associated with bodymass index in men fromthe National Heart, Lung, and Blood Institute Family Heart Study (2004) The American Journal of Human Genetics, 75 (2), pp. 220-230He, J., Xi, B., Ruiter, R., Association of LEP G2548A and LEPR Q223R polymorphisms with cancer susceptibility: Evidence froma meta-analysis (2013) PLoS ONE, 8 (10)Furusawa, T., Naka, I., Yamauchi, T., The Q223R polymorphism in LEPR is associated with obesity in Pacific Islanders (2010) Human Genetics, 127 (3), pp. 287-294Saukko, M., Kesäniemi, Y.A., Ukkola, O., Leptin receptor Lys109Arg and Gln223Arg polymorphisms are associated with early atherosclerosis (2010) Metabolic Syndrome and Related Disorders, 8 (5), pp. 425-430Lucas, A., Granada, M.L., Olaizola, I., Leptin and thyrotropin relationship is modulated by smoking status in euthyroid subjects (2013) Thyroid, 23 (8), pp. 964-970Duntas, L.H., Biondi, B., The interconnections between obesity, thyroid function, and autoimmunity: Themultifold role of leptin (2013) Thyroid, 23 (6), pp. 646-653Marzullo, P., Minocci, A., Tagliaferri, M.A., Investigations of thyroid hormones and antibodies in obesity: Leptin levels are associated with thyroid autoimmunity independent of bioanthropometric, hormonal, and weight-related determinants (2010) Journal of Clinical Endocrinology and Metabolism, 95 (8), pp. 3965-3972Guzel, S., Seven, A., Guzel, E.C., Buyuk, B., Celebi, A., Aydemir, B., Visfatin, leptin, and TNF-α: Interrelated adipokines in insulin-resistant clinical and subclinical hypothyroidism (2013) Endocrine Research, 38 (3), pp. 184-194Mammès, O., Betoulle, D., Aubert, R., Herbeth, B., Siest, G., Fumeron, F., Association of the G-2548A polymorphism in the 5' region of the LEP gene with overweight (2000) Annals of Human Genetics, 64 (5), pp. 391-394Portoles, O., Sorli, J.V., Frances, F., Effect of genetic variation in the leptin gene promoter and the leptin receptor gene on obesity risk in a population-based case-control study in Spain (2006) European Journal of Epidemiology, 21 (8), pp. 605-612Liu, C., Liu, L., Polymorphisms in three obesity-related genes (LEP, LEPR, and PON1) and breast cancer risk: A metaanalysis (2011) Tumour Biology, 32 (6), pp. 1233-1240Hoffsted, J., Eriksson, P., Mottagui-Tabar, S., Arner, P., A polymorphism in the leptin promoter region (-2548 G/A) influences gene expression and adipose tissue secretion of leptin (2002) Hormone and Metabolic Research, 34 (7), pp. 355-359Murugesan, D., Arunachalam, T., Ramamurthy, V., Subramanian, S., Association of polymorphisms in leptin receptor gene with obesity and type 2 diabetes in the local population of Coimbatore (2010) Indian Journal of Human Genetics, 16 (2), pp. 72-77Quinton, N.D., Lee, A.J., Ross, R.J.M., Eastell, R., Blakemore, A.I.F., A single nucleotide polymorphism (SNP) in the leptin receptor is associated with BMI, fatmass and leptin levels in postmenopausal Caucasian women (2001) Human Genetics, 108 (3), pp. 233-236Mattevi, V.S., Zembrzuski, V.M., Hutz, M.H., Association analysis of genes involved in the leptin-signaling pathway with obesity in Brazil (2002) International Journal of Obesity, 26 (9), pp. 1179-1185Yiannakouris, N., Yannakoulia, M., Melistas, L., Chan, J.L., Klimis-Zacas, D., Mantzoros, C.S., TheQ223Rpolymorphism of the leptin receptor gene is significantly associated with obesity and predicts a small percentage of bodyweight and body composition variability (2001) Journal of Clinical Endocrinology and Metabolism, 86 (9), pp. 4434-4439Stefan, N., Vozarova, B., Del Parigi, A., The Gln223Arg polymorphism of the leptin receptor in Pima Indians: Influence on energy expenditure, physical activity and lipid metabolism (2002) International Journal of Obesity, 26 (12), pp. 1629-1632Chiu, K.C., Chu, A., Chuang, L.-M., Saad, M.F., Association of leptin receptor polymorphism with insulin resistance (2004) European Journal of Endocrinology, 150 (5), pp. 725-729Chu, A., Chuang, L.M., Saad, M., Chiu, K., Association of the Q223R polymorphism of the leptin receptor gene with insulin resistance and metabolic syndrome (2003) Diabetes, 52, p. A510Pimentel Duarte, S.F., Francischetti, E.A., Genelhu-Abreu, V., P. Q223R leptin receptor polymorphism associated with obesity in Brazilianmultiethnic subjects (2006) The American Journal of Human Biology, 18 (4), pp. 448-453Wauters, M., Mertens, I., Chagnon, M., Polymorphisms in the leptin receptor gene, body composition and fat distribution in overweight and obese women (2001) International Journal of Obesity, 25 (5), pp. 714-720Ogawa, T., Hirose, H., Yamamoto, Y., Relationships between serum soluble leptin receptor level and serum leptin and adiponectin levels, insulin resistance index, lipid profile, and leptin receptor gene polymorphisms in the Japanese population (2004) Metabolism: Clinical and Experimental, 53 (7), pp. 879-885Fairbrother, U.L., Tankó, L.B., Walley, A.J., Christiansen, C., Froguel, P., Blakemore, A.I.F., Leptin receptor genotype at Gln223Arg is associated with body composition, BMD, and vertebral fracture in postmenopausal Danish women (2007) Journal of Bone and Mineral Research, 22 (4), pp. 544-550Salopuro, T., Pulkkinen, L., Lindström, J., Genetic variation in leptin receptor gene is associated with type 2 diabetes and body weight: The Finnish Diabetes Prevention Study (2005) International Journal of Obesity, 29 (10), pp. 1245-1251Wauters, M., Mertens, I., Rankinen, T., Chagnon, M., Bouchardt, C., Van Gaal, L., Leptin receptor gene polymorphisms are associated with insulin in obese women with impaired glucose tolerance (2001) Journal of Clinical Endocrinology and Metabolism, 86 (7), pp. 3227-3232Park, K.S., Shin, H.D., Park, B.L., Polymorphisms in the leptin receptor (LEPR)-putative association with obesity and T2DM (2006) Journal of Human Genetics, 51 (2), pp. 85-91Han, C.-Z., Du, L.-L., Jing, J.-X., Associations among lipids, leptin, and leptin receptor geneGin223Arg polymorphisms and breast cancer in China (2008) Biological Trace Element Research, 126 (1-3), pp. 38-48Okobia, M.N., Bunker, C.H., Garte, S.J., Leptin receptor Gln223Arg polymorphism and breast cancer risk in Nigerian women: A case control study (2008) BMC Cancer, 8He, B.-S., Pan, Y.-Q., Zhang, Y., Xu, Y.-Q., Wang, S.-K., Effect of LEPR Gln223Arg polymorphism on breast cancer risk in different ethnic populations: A meta-analysis (2012) Molecular Biology Reports, 39 (3), pp. 3117-3122Lin, D.W., Fitz Gerald, L.M., Fu, R., Genetic variants in the LEPR, CRY1, RNASEL, IL4, and ARVCF genes are prognostic markers of prostate cancer-specific mortality (2011) Cancer Epidemiology, Biomarkers & Prevention, 20 (9), pp. 1928-1936Li, Y.L., Geng, J.L., Wang, Y., The role of leptin receptor gene polymorphisms in determining the susceptibility and prognosis of NSCLC in Chinese patients (2012) Journal of Cancer Research and Clinical Oncology, 138 (2), pp. 311-316Wazir, U., Al Sarakbi, W., Jiang, W.G., Mokbel, K., Evidence of an autocrine role for leptin and leptin receptor in human breast cancer (2012) CancerGenomics and Proteomics, 9 (6), pp. 383-388Li, L., Lee, K.J., Choi, B.C., Baek, K.H., Relationshipbetween leptin receptor and polycystic ovary syndrome (2013) Gene, 527 (1), pp. 71-74Friedlander, Y., Li, G., Fornage, M., Candidate molecular pathway genes related to appetite regulatory neural network, adipocyte homeostasis and obesity: Results from the CARDIA Study (2010) Annals of Human Genetics, 74 (5), pp. 387-39