Pressure ulcer prevalence in intensive care patients: a cross-sectional study

Background  Pressure ulcers are a potential complication for intensive care patients and their prevention is a major issue in nursing care. Therefore, this study aims to assess pressure ulcer prevalence in intensive care patients, patients' characteristics and preventive measures related to pressure ulcer prevalence in intensive care patients and to determine the most common body sites of pressure ulcers.
Method  The research design was a cross-sectional study. The sample consisted of 1760 patients (298 in 2002, 408 in 2003, 453 in 2004, 368 in 2005 and 233 participants in 2006) from surgical, medical and interdisciplinary intensive care.
Results  The results revealed a mean prevalence rate of ±30% from 2002 to 2005 while it considerably decreased down to 16.2% in 2006. Half of the pressure ulcers were of grade 1. Furthermore, a significant relation was found between the presence of pressure ulcers and age ( P  ≤ 0.022), Braden score ( P  ≤ 0.01) and bowel incontinence ( P  ≤ 0.01).
Conclusion  It is crucial to select appropriate and applicable preventive material/devices and nursing care measures. Moreover, factors related to the presence of pressure ulcers should be taken into consideration in order to prevent development of further pressure ulcers.     

CYP1B1 mutation profile of Iranian primary congenital glaucoma patients and associated haplotypes

The mutation spectrum of CYP1B1 among 104 primary congenital glaucoma patients of the genetically heterogeneous Iranian population was investigated by sequencing. We also determined intragenic single nucleotide polymorphism (SNP) haplotypes associated with the mutations and compared these with haplotypes of other populations. Finally, the frequency distribution of the haplotypes was compared among primary congenital glaucoma patients with and without CYP1B1 mutations and normal controls. Genotype classification of six high-frequency SNPs was performed using the PHASE 2.0 software. CYP1B1 mutations in the Iranian patients were very heterogeneous. Nineteen nonconservative mutations associated with disease, and 10 variations not associated with disease were identified. Ten mutations and three variations not associated with disease were novel. The 13 novel variations make a notable contribution to the approximately 70 known variations in the gene. CYP1B1 mutations were identified in 70% of the patients. The four most common mutations were G61E, R368H, R390H, and R469W, which together constituted 76.2% of the CYP1B1 mutated alleles found. Six unique core SNP haplotypes were identified, four of which were common to the patients with and without CYP1B1 mutations and controls studied. Three SNP blocks determined the haplotypes. Comparison of haplotypes with those of other populations suggests a common origin for many of the mutations.     

Mitochondrial serine protease HTRA2 p.G399S in a kindred with essential tremor and Parkinson disease

Essential tremor is one of the most frequent movement disorders of humans and can be associated with substantial disability. Some but not all persons with essential tremor develop signs of Parkinson disease, and the relationship between the conditions has not been clear. In a six-generation consanguineous Turkish kindred with both essential tremor and Parkinson disease, we carried out whole exome sequencing and pedigree analysis, identifying HTRA2 p.G399S as the allele likely responsible for both conditions. Essential tremor was present in persons either heterozygous or homozygous for this allele. Homozygosity was associated with earlier age at onset of tremor (P < 0.0001), more severe postural tremor (P < 0.0001), and more severe kinetic tremor (P = 0.0019). Homozygotes, but not heterozygotes, developed Parkinson signs in the middle age. Among population controls from the same Anatolian region as the family, frequency of HTRA2 p.G399S was 0.0027, slightly lower than other populations. HTRA2 encodes a mitochondrial serine protease. Loss of function of HtrA2 was previously shown to lead to parkinsonian features in motor neuron degeneration (mnd2) mice. HTRA2 p.G399S was previously shown to lead to mitochondrial dysfunction, altered mitochondrial morphology, and decreased protease activity, but epidemiologic studies of an association between HTRA2 and Parkinson disease yielded conflicting results. Our results suggest that in some families, HTRA2 p.G399S is responsible for hereditary essential tremor and that homozygotes for this allele develop Parkinson disease. This hypothesis has implications for understanding the pathogenesis of essential tremor and its relationship to Parkinson disease.Essential tremor is one of the most frequent movement disorders in humans (1). It is characterized primarily by postural or kinetic tremor of the arms and hands, but head, legs, voice, and other regions of the body may also be affected (2). The worldwide prevalence is 0.9%, increasing to more than 4% in elderly populations (1). Familial essential tremor is genetically heterogeneous. Genetic linkage studies of multiply affected families revealed three genomic regions segregating with the condition, on chromosomes 3q13 [ETM1; Online Mendelian Inheritance in Man (OMIM) 190300], 2p22-24 (ETM2; OMIM 602134), and 6p23 (ETM3; OMIM 611456) (3–5). No clearly causal mutations have been identified in these regions, although the common variant DRD3 p.S9G in the ETM1 region has been proposed as a risk factor and HS1BP3 p.A265G in the ETM2 region appeared in two multiply affected families (6, 7). Genomewide association studies of essential tremor reported associations with common variants in an intron of LINGO1 and in an intron of SLC1A2 (8–10). Recently, DNAJC13 p.N855S, which had been identified in Parkinson disease patients, was also found in two unrelated patients with essential tremor (11). Nonsense mutation p.Q290X in the RNA-binding protein FUS was identified by whole exome sequencing in a large family with essential tremor (ETM4; OMIM 614782) (12). Screening other subjects with essential tremor for FUS revealed two rare missense variants, suggesting that mutations in FUS explain a subset of cases with the condition (13, 14).In this study, we examined a six-generation family segregating essential tremor, and in multiple relatives, essential tremor as a feature of Parkinson disease. We carried out whole exome sequencing of genomic DNA from three severely affected family members and subsequent pedigree analysis to identify the genetic basis of essential tremor and Parkinson disease in the family.     

Cost-Effectiveness of Endovascular Versus Open Repair of Abdominal Aortic Aneurysm: A Systematic Review

Cardiovascular Drugs and Therapy - Abdominal aortic aneurysm (AAA) is a life-threatening condition which, in the absence of increasing diameter or rupture, often remains asymptomatic, and a...     

Arthritis and osteonecrosis in a patient with thrombophilia

This case report describes a very rare entity of thrombophilia manifesting as persistent arthritis and digital ulcers. A 9-year-old Egyptian girl presented with a 2-year history of persistent arthritis and digital ulcers. The case was followed up after 4 years. The clinical manifestations and laboratory investigations are recorded. Thrombophilia with partial protein C deficiency appeared to be responsible for the clinical manifestations with underlying ipsilateral osteonecrosis of patella and calcaneum and resorption of the terminal phalanges. Her older sister showed the same picture with additional pulmonary hypertension. In conclusion, arthritis and osteonecrosis appear as a rare presentation of thrombophilia and protein C deficiency, and ignorance of this may lead to misdiagnosis or confusion with other childhood rheumatic diseases.     

The clinical patterns of myalgia in children with familial Mediterranean fever

OBJECTIVES: To study the frequency and clinical patterns of myalgia in a defined group of children with familial Mediterranean fever (FMF). METHODS: A prospective 4-year (September 1995-September 1999) study of children with FMF seen in the pediatric FMF clinic of Jordan University teaching hospital. Diagnosis of FMF was made according to published criteria. Once the diagnosis of FMF and myalgia was made, details about myalgia were collected by interview with the child and his/her parents and entered into a special study form. RESULTS: Of 264 children with FMF seen over the study period, 65 (25%) developed myalgia. Three clinical patterns of myalgia were identified: the spontaneous pattern, the exercise-induced pattern, and the protracted febrile myalgia syndrome (PFMS), seen in 8%, 81%, and 11% of patients, respectively. The three patterns differed in the severity of pain, height of fever, and duration of the episode. In 33 children with the exercise-induced myalgia, in which response to colchicine could be reliably assessed, a favorable response was achieved in 97%. Three children with the PFMS had a dramatic response to corticosteroids. CONCLUSIONS: Myalgia in children with FMF is common and can follow three different clinical patterns.     

Pam3CSK4 enhanced beta cell loss and diabetogenesis: The roles of IFN-gamma and IL-17

Toll like receptors are primary sensors of both innate and adaptive immune systems. They activate APCs and influence T-cell function in inflammatory autoimmune response. Studies have shown that TLR manipulation may lead to either tolerance or trigger autoimmunity. Using diabetogenic and subdiabetogenic multiple low doses of streptozotocin, we demonstrate here that Pam3 CYS-CK₄ a TLR-2 agonist, enhances and promotes diabetes in C57BL/6 male mice following increased apoptosis of β islet cells. FACS analysis of isolated pancreatic lymph node cells revealed significant increased number of macrophages, dendritic cells, CD4⁺ TNF-α⁺, CD4⁺ IFN-γ⁺ and most significantly, CD4⁺ IL-17⁺ and reduced number of CD25⁺Fox p3⁺ T cells after Pam3CSK₄ treatment. Genetic deletion of IFN-γ prevents whereas deletion of IL-17 reduced severity of Pam3CSK₄-induced enhancement of diabetes. TLR-2 agonist-enhanced diabetogenesis is also influenced by enhanced influx of antigen presenting cells and suppression of regulatory T cell activity.     

Correction: The β-cyclodextrin-modified nanosized ZSM-5 zeolite as a carrier for curcumin

Correction for ‘The β-cyclodextrin-modified nanosized ZSM-5 zeolite as a carrier for curcumin’ by Shahin Amani et al., RSC Adv., 2019, 9, 32348–32356, DOI: 10.1039/C9RA04739E.

The authors regret that the names of the authors were listed incorrectly in the original article. The corrected author list is as shown above.The Royal Society of Chemistry apologises for these errors and any consequent inconvenience to authors and readers.