2m-cycle systems of K2m+1/C-m

For all m greater than or equal to 3 the edges of complete graph on 2m + 1 vertices can he partitioned into m 2m-cycles and an m-cycle.

The metamorphosis of lambda-fold K-3,K-3-designs into lambda-fold 6-cycle systems

In this paper necessary and sufficient conditions are given for the metamorphosis of a lambda-fold K-3,K-3-design of order n into a lambda-fold 6-cycle system of order n, by retaining one 6-cycle subgraph from each copy of K-3,K-3, and then rearranging the set of all the remaining edges, three from each K-3,K-3, into further 6-cycles so that the result is a lambda-fold 6-cycle system.

Synthesis of mucoadhesive thiol-bearing microgels from 2-(acetylthio)ethylacrylate and 2-hydroxyethylmethacrylate: novel drug delivery systems for chemotherapeutic agents to the bladder

Thiol-bearing microgels have been synthesised from copolymerisation of 2-(acetylthio)ethylacrylate and 2-hydroxyethylmethacrylate, and subsequent deprotection using sodium thiomethoxide. The concentration of thiol groups on these microgels could be tailored by use of different molar ratios of the two monomers. These thiol-bearing microgels were shown to adhere to ex vivo porcine urinary bladder, which was correlated with their level of thiolation. By simply mixing solutions of thiol-bearing microgels and doxorubicin, high levels of drug loading into the microgels could be achieved. Thiol-bearing microgels controlled the release of doxorubicin in a time-dependent manner over several hours. These doxorubicin-loaded thiol-bearing microgels could have application in the treatment of early-stage bladder cancers. The method used represents a new ‘bottom-up’ approach for the synthesis of novel mucoadhesive microgels.

X1X1X2X2/X1X2Y sex chromosome systems in the Neotropical Gymnotiformes electric fish of the genus Brachyhypopomus

Several types of sex chromosome systems have been recorded among Gymnotiformes, including male and female heterogamety, simple and multiple sex chromosomes, and different mechanisms of origin and evolution. The ₁X₁X₂X₂/X₁X₂Y systems identified in three species of this order are considered homoplasic for the group. In the genus Brachyhypopomus, only B. gauderio presented this type of system. Herein we describe the karyotypes of Brachyhypopomus pinnicaudatus and B. n. sp. FLAV, which have an X₁X₁X₂X₂/X₁X₂Y sex chromosome system that evolved via fusion between an autosome and the Y chromosome. The morphology of the chromosomes and the meiotic pairing suggest that the sex chromosomes of B. gauderio and B. pinnicaudatus have a common origin, whereas in B. n. sp. FLAV the sex chromosome system evolved independently. However, we cannot discard the possibility of common origin followed by distinct processes of differentiation. The identification of two new karyotypes with an X₁X₁X₂X₂/X₁X₂Y sex chromosome system in Gymnotiformes makes it the most common among the karyotyped species of the group. Comparisons of these karyotypes and the evolutionary history of the taxa indicate independent origins for their sex chromosomes systems. The recurrent emergence of the X₁X₁X₂X₂/X₁X₂Y system may represent sex chromosomes turnover events in Gymnotiformes.

Comparative study of bone repair in mandibular body osteotomy between metallic and absorbable 2.0 mm internal fixation systems. Histological and histometric analysis in dogs: a pilot study

The objective of this study was to compare the bone repair along a mandibular body osteotomy stabilized with 2.0 mm absorbable and metallic systems. 12 male, adult mongrel dogs were divided into two groups (metallic and absorbable) and subjected to unilateral osteotomy between the mandibular third and fourth premolars, which was stabilized by applying two 4-hole plates. At 2 and 18 weeks, three dogs from each group were killed and the osteotomy sites were removed and divided equally into three parts: the upper part was labelled the tension third (TT), the lower part the compression third (CT), and the part between the TT and CT the intermediary third (IT). Regardless of the treatment system, union between the fragments was observed at 18 weeks and the CT showed more advanced stages of bone repair than the TT. Histometric analysis did not reveal any significant differences among the 3 parts or systems in the distance between bone fragments at 2 weeks. Although at 18 weeks the proportions of newly formed bone did not differ among TT, IT and CT, significantly enhanced bone formation was observed in all sections for the metallic group. The patterns of repair were distinct between treatments.

Configurations in 4-cycle systems

A 4-cycle system of order n, denoted by 4CS(n), exists if and only if nequivalent to1 (mod 8). There are four configurations which can be formed by two 4-cycles in a 4CS(n). Formulas connecting the number of occurrences of each such configuration in a 4CS(n) are given. The number of occurrences of each configuration is determined completely by the number d of occurrences of the configuration D consisting of two 4-cycles sharing a common diagonal. It is shown that for every nequivalent to1 (mod 8) there exists a 4CS(n) which avoids the configuration D, i.e. for which d=0. The exact upper bound for d in a 4CS(n) is also determined.

Understanding Ten-Eleven Translocation-2 in Hematological and Nervous Systems

I proposed the study of two distinct aspects of Ten-Eleven Translocation 2 (TET2) protein for understanding specific functions in different body systems. In Part I, I characterized the molecular mechanisms of Tet2 in the hematological system. As the second member of Ten-Eleven Translocation protein family, TET2 is frequently mutated in leukemic patients. Previous studies have shown that the TET2 mutations frequently occur in 20% myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN), 10% T-cell lymphoma leukemia and 2% B-cell lymphoma leukemia. Genetic mouse models also display distinct phenotypes of various types of hematological malignancies. I performed 5-hydroxymethylcytosine (5hmC) chromatin immunoprecipitation sequencing (ChIP-Seq) and RNA sequencing (RNA-Seq) of hematopoietic stem/progenitor cells to determine whether the deletion of Tet2 can affect the abundance of 5hmC at myeloid, T-cell and B-cell specific gene transcription start sites, which ultimately result in various hematological malignancies. Subsequent Exome sequencing (Exome-Seq) showed that disease-specific genes are mutated in different types of tumors, which suggests that TET2 may protect the genome from being mutated. The direct interaction between TET2 and Mutator S Homolog 6 (MSH6) protein suggests TET2 is involved in DNA mismatch repair. Finally, in vivo mismatch repair studies show that the loss of Tet2 causes a mutator phenotype. Taken together, my data indicate that TET2 binds to MSH6 to protect genome integrity. In Part II, I intended to better understand the role of Tet2 in the nervous system. 5-hydroxymethylcytosine regulates epigenetic modification during neurodevelopment and aging. Thus, Tet2 may play a critical role in regulating adult neurogenesis. To examine the physiological significance of Tet2 in the nervous system, I first showed that the deletion of Tet2 reduces the 5hmC levels in neural stem cells. Mice lacking Tet2 show abnormal hippocampal neurogenesis along with 5hmC alternations at different gene promoters and corresponding gene expression downregulation. Through the luciferase reporter assay, two neural factors Neurogenic differentiation 1 (NeuroD1) and Glial fibrillary acidic protein (Gfap) were down-regulated in Tet2 knockout cells. My results suggest that Tet2 regulates neural stem/progenitor cell proliferation and differentiation in adult brain.

Understanding ten-eleven translocation-2 in hematological and nervous systems

I proposed the study of two distinct aspects of Ten-Eleven Translocation 2 (TET2) protein for understanding specific functions in different body systems. ^ In Part I, I characterized the molecular mechanisms of Tet2 in the hematological system. As the second member of Ten-Eleven Translocation protein family, TET2 is frequently mutated in leukemic patients. Previous studies have shown that the TET2 mutations frequently occur in 20% myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN), 10% T-cell lymphoma leukemia and 2% B-cell lymphoma leukemia. Genetic mouse models also display distinct phenotypes of various types of hematological malignancies. I performed 5-hydroxymethylcytosine (5hmC) chromatin immunoprecipitation sequencing (ChIP-Seq) and RNA sequencing (RNA-Seq) of hematopoietic stem/progenitor cells to determine whether the deletion of Tet2 can affect the abundance of 5hmC at myeloid, T-cell and B-cell specific gene transcription start sites, which ultimately result in various hematological malignancies. Subsequent Exome sequencing (Exome-Seq) showed that disease-specific genes are mutated in different types of tumors, which suggests that TET2 may protect the genome from being mutated. The direct interaction between TET2 and Mutator S Homolog 6 (MSH6) protein suggests TET2 is involved in DNA mismatch repair. Finally, in vivo mismatch repair studies show that the loss of Tet2 causes a mutator phenotype. Taken together, my data indicate that TET2 binds to MSH6 to protect genome integrity. ^ In Part II, I intended to better understand the role of Tet2 in the nervous system. 5-hydroxymethylcytosine regulates epigenetic modification during neurodevelopment and aging. Thus, Tet2 may play a critical role in regulating adult neurogenesis. To examine the physiological significance of Tet2 in the nervous system, I first showed that the deletion of Tet2 reduces the 5hmC levels in neural stem cells. Mice lacking Tet2 show abnormal hippocampal neurogenesis along with 5hmC alternations at different gene promoters and corresponding gene expression downregulation. Through the luciferase reporter assay, two neural factors Neurogenic differentiation 1 (NeuroD1) and Glial fibrillary acidic protein (Gfap) were down-regulated in Tet2 knockout cells. My results suggest that Tet2 regulates neural stem/progenitor cell proliferation and differentiation in adult brain.^

The extended metamorphosis of a complete bipartite design into a cycle system

A K-t,K-t-design of order n is an edge-disjoint decomposition of K-n into copies of K-t,K-t. When t is odd, an extended metamorphosis of a K-t,K-t-design of order n into a 2t-cycle system of order n is obtained by taking (t - 1)/2 edge-disjoint cycles of length 2t from each K-t,K-t block, and rearranging all the remaining 1-factors in each K-t,K-t block into further 2t-cycles. The 'extended' refers to the fact that as many subgraphs isomorphic to a 2t-cycle as possible are removed from each K-t,K-t block, rather than merely one subgraph. In this paper an extended metamorphosis of a K-t,K-t-design of order congruent to 1 (mod 4t(2)) into a 2t-cycle system of the same order is given for all odd t > 3. A metamorphosis of a 2-fold K-t,K-t-design of any order congruent to 1 (mod 4t(2)) into a 2t-cycle system of the same order is also given, for all odd t > 3. (The case t = 3 appeared in Ars Combin. 64 (2002) 65-80.) When t is even, the graph K-t,K-t is easily seen to contain t/2 edge-disjoint cycles of length 2t, and so the metamorphosis in that case is straightforward. (C) 2004 Elsevier B.V. All rights reserved.