Modified Limberg transposition flap in the treatment of pilonidal sinus disease.

BACKGROUND: Pilonidal sinus disease (PSD) is a common problem in surgical practice. Different non-surgical and surgical methods have been used for treating PSD. Flap techniques including the Limberg flap have become more popular in recent years. A modified Limberg flap was used to reduce the problems of skin maceration and recurrence associated with the conventional Limberg flap technique. The aim of this retrospective study was to assess the effectiveness of the modified Limberg flap technique for PSD. METHODS: Medical records of 94 patients with PSD who had been treated with a modified Limberg flap between December 2006 and 2009 were evaluated. The patients' age, sex, duration of preoperative symptoms, operative time, mean hospital stay, postoperative complications, wound infection rate, maceration rate and recurrence rate, time until return to work, time until sitting on the toilet without pain, hypoesthesia in the gluteal region, and satisfaction score were recorded during follow-up or at the last interview. Clinical data were obtained at the end of the 5th postoperative day and at 1, 3, 6, and 12 months following surgery. RESULTS: There were 83 male and 11 female patients. The mean operative time was 38.95 ± 6.77 min (range 30-67 min). All patients were followed up longer than 12 months, and the mean follow-up period was 30.97 ± 12.7 months (range 12-54 months). While wound dehiscence was observed in only one patient, we did not detect any case of flap necrosis. Two cases of seroma were observed. Wound infection was detected in 5 patients (5.3%). Surgical drainage was performed in 2 cases. Another 3 patients were treated with oral antibiotics. Maceration of the surgical incision site was detected in 8 patients (8.5%) who were all successfully treated with conservative measures. There were 4 patients (4.2%) with recurrence in this series. CONCLUSIONS: When compared with the available data on use of the conventional Limberg flap for PSD, our results suggest that use of the modified Limberg flap is associated with a lower maceration and recurrence rate, and greater patient satisfaction.

Evolutionary relationships among proteins encoded by the regulator of complement activation gene cluster.

Evolutionary relationships among members of the regulator of complement activation (RCA) gene cluster were analyzed using neighbor-joining and parsimony methods of phylogenetic tree inference. We investigated the structural and functional similarities among short consensus repeats (SCRs) of the following human proteins: the alpha chain of the C4b-binding protein (C4bpalpha), factor H (FH), factor H-related proteins (FHR-1 through FHR-4), complement receptors type 1 (CR1) and type 2 (CR2), the CR1-like protein (CR1L), membrane cofactor protein (MCP), decay accelerating factor (DAF), and the sand bass proteins, the cofactor protein (SBP1) and its homolog, the cofactor-related protein (SBCRP-1). Also included are the beta chain of the human C4b-binding protein (C4bpbeta) and the b subunit of human blood-clotting factor XIII (FXIIIb). Our results indicate that the human plasma complement regulators, FH and C4bpalpha, fall into two distinct groups on the basis of their sequence divergence. Homology among RCA proteins is in agreement with their chromosomal location, with the exception of C4bpbeta. The evolutionary relationships among individual short consensus repeats are confirmed by the exon/intron structure of the RCA members. Structural similarities among repeats of the RCA proteins correlate with their functional activities and demonstrate the importance of the N-terminal SCRs.

Psoralen cross-linking as probe of torsional tension and topological domain size in vivo.

DNA within a cell is organized with unrestrained torsional tension, and each molecule is divided into multiple individual topological domains. Psoralen photobinding can be used as an assay for supercoiling and topological domain size in living cells. Psoralen photobinds to DNA at a rate nearly linearly proportional to superhelical density. Comparison of the rate of photobinding to supercoiled and relaxed DNA in cells provides a measure of superhelical density. For this, in vivo superhelical tension is relaxed by the introduction of nicks by either ionizing radiation or photolysis of bromodeoxyuridine in the DNA. Since nicks are introduced in a random fashion, the distribution of nicks is described by a Poisson distribution. Thus, after nicking, the fraction of topological domains containing no nicks is described by the zero term of the Poisson distribution. From measurement of the number of nicks introduced in the DNA and the fraction of torsional tension remaining, an average topological domain size can be estimated. Using this logic, procedures were designed and described for measuring supercoiling and domain size at specific sites in eukaryotic genomes.

Computer simulation of expansions of DNA triplet repeats in the fragile X syndrome and Huntington's disease.

The expansion of DNA triplet repeats has been shown to be responsible for about a dozen hereditary diseases. In this paper we are concerned with a computer model of such expansion, applied to the fragile X syndrome and Huntington's disease, for which enough quantitative data have been collected. The nucleotide sequence associated with the fragile X consists of CGG repeats and is located inside the FMR1 gene. In normal individuals there is a variable number of triplet repeats less than 60; in asymptomatic carriers the number of repeats is 60-200 (premutation). From the premutation range, the number of triplet repeats can increase within one generation to more than 200 producing affected individuals. In Huntington's disease the CAG repeats are located inside the HD gene. In normal individuals the number of repeats varies from around 11, up to 34. In the intermediate range (34-37 repeats), the mutability is increased, frequently leading to alleles of more than 37 repeats, and the disease phenotype. The rapid increase of the number of triplet repeats in affected individuals has been proposed to be due to the formation of folded DNA structures (hairpins) and their repair or misrepair. In order to determine if this proposed mechanism is adequate to account for the rapid increase of repeats and the large number of repeats in affected individuals we developed a mathematical model that includes the known mechanisms of hairpin formation, and strand synthesis and repair. Simulations based on the model using realistic probabilities of hairpin formation produced results that corresponded with the observed range of repeats and transition probabilities from normal to affected individuals. Similar modelling has been published for the Huntington's disease data. However, in this paper we demonstrate that a uniform approach works for fragile X and Huntington's disease, although the detailed assumptions of the model have to be different. These difference provide insight into the mechanisms of expansion in both cases. Among these insights is that an apparent threshold in the number of repeats for rapid expansion, and the preference for expansion over contraction, may be accounted for by relative probabilities of hairpin formation, replication, slippage and repair.

Development of a faculty research interest resource.

We have developed a faculty research interests resource by "mining" MEDLINE for relationships that are not directly queryable through the normal MEDLINE schema. Faculty citations are retrieved and World-Wide Web pages built to interconnect authors, their citations, and the MeSH terms that have been assigned to these citations. The design and development of the resource are discussed and examples of the results illustrated.

[Q fever in the western region of Ukraine]. / Likhoradka Ku v zapadnom regione Ukrainy.

Multiple natural and mixed foci of Q fever have been revealed at the territory of six administrative regions of the western part of the Ukraine. Coxiella burnetii strains have been isolated from small animals and ticks, the specific features of their ecology in Poles'e and forest-steppe zones have been determined. The necessity of the study of natural foci of Q fever at not yet surveyed territories for at least 3-4 years has been substantiated.

[The diagnosis of rickettsioses in patients under therapy]. / Diahnostyka ryketsioziv u khvorykh terapevtychnoho profiliu.

A serological study of 92 patients with rickettsiosis, revealed in the blood serum of 19 patients antibodies to the pathogens of Q-fever or typhoid fever. In three patients the character of distribution of immunoglobulins of different classes corresponded to the chronic course of rickettsia infection. Patients of the therapeutic profile from infections foci should be examined for rickettsiosis.

[Clinico-epidemiological characteristics of Q fever in the Carpathian region]. / Kliniko-épidemiologicheskaia kharakteristika Ku-likhoradki v Prikarpat'e.

The study of the specific epidemiological and clinical features of Q fever revealed the existence of an active focus of infection among humans due to their contacts with agricultural animals in one of the districts of the region. The focus was manifested by group morbidity among the cattle-tending personnel of a dairy farm. The source of this infection was cattle. The infection was transferred mainly through the air. The disease took a moderately severe course. The study of the rickettsial contamination of humans, animals and ticks suggested the presence of the active epidemic process and made it possible to work out concrete antiepidemic measures.