ABSTRACT
Long-pulsed 1064-nm (LP1064) and 755-nm (LP755) lasers have been demonstrated as effective treatments for leg veins. However, few studies of these treatments on Asian skin type as well as direct comparison between two methods were reported. The aim of this study was to compare the clinical efficacy and safety of LP1064 with LP755 in the treatment of C1 leg veins on skin type IV patients. Patients with symmetric matched areas C1 leg veins were treated with single session of LP1064 for the right and LP755 for the left. Treated areas of every patient were divided into matrices of 2 × 2 cm squares. Vessels in the highest density squares were subjected to evaluation. Spot sizes were 5 mm fixed. Pulse durations and fluences were according to vessel diameters and endpoints, respectively. The clearances were evaluated at 1 and 3 months post treatment. Side effects were recorded immediately, 10 min, 24 h, and 1 and 3 months after treatment. Twenty-two patients were enrolled with total 96 vessels from 22 selected squares in the right and 106 vessels from 22 selected squares in the left. At 1-month follow-up, the clearances of LP1064 and LP755 were not significantly different (71.87% and 71.69%, respectively; p = 0.99). At 3-month follow-up, the efficacies were constant and no recurrence occurred. Pain levels of both methods were moderate and significantly lower in LP755. These findings suggest that LP1064 and LP755 laser treatments were comparatively effective and safe for C1 leg veins of skin type IV patients.
Subject(s)
Laser Therapy , Leg/radiation effects , Telangiectasis/surgery , Adult , Humans , Laser Therapy/adverse effects , Male , Middle Aged , Safety , Treatment OutcomeABSTRACT
BACKGROUND: Large-scale, multisite studies in which researchers evaluate patient- and systems-level factors associated with pediatric asthma exacerbation outcomes are lacking. We sought to investigate patient-level risks and system-level practices related to physiologic readiness for discharge (PRD) in the prospective Ohio Pediatric Asthma Repository. METHODS: Participants were children ages 2 to 17 years admitted to an Ohio Pediatric Asthma Repository hospital for asthma exacerbation. Demographics, disease characteristics, and individual hospital practices were collected. The primary outcome was PRD timing (hours from admission or emergency department [ED] presentation until the first 4-hour albuterol spacing). RESULTS: Data for 1005 participants were available (865 ED presentations). Several nonstandard care practices were associated with time to PRD (P < .001). Continuous pulse oximetry was associated with increased time to PRD (P = .004). ED dexamethasone administration was associated with decreased time to PRD (P < .001) and less ICU admittance and intravenous steroid use (P < .0001). Earlier receipt of chest radiograph, antibiotics, and intravenous steroids was associated with shorter time to PRD (P < .05). Care practices associated with shorter time to PRD varied markedly by hospital. CONCLUSIONS: Substantial variation in care practices for inpatient asthma treatment exists among children's hospital systems in Ohio. We found several modifiable, system-level factors and therapies that contribute to PRD that warrant further investigation to identify the best and safest care practices. We also found that there was no standardized measure of exacerbation severity used across the hospitals. The development of such a tool is a critical gap in current practice and is needed to enable definitive comparative effectiveness studies of the management of acute asthma exacerbation.
Subject(s)
Anti-Asthmatic Agents/administration & dosage , Asthma/therapy , Emergency Service, Hospital , Guideline Adherence , Hospitalization/statistics & numerical data , Patient Discharge , Adolescent , Asthma/epidemiology , Asthma/physiopathology , Child , Child, Preschool , Dexamethasone/administration & dosage , Female , Humans , Male , Ohio/epidemiology , Patient Discharge/statistics & numerical data , Practice Guidelines as Topic , Prednisone/administration & dosage , Prospective Studies , Radiography, Thoracic/statistics & numerical dataABSTRACT
AIM: To determine the vaccination rates in pediatric immunosuppression-dependent inflammatory bowel disease (IBD) and review the safety and efficacy of vaccinations in this population. METHODS: The electronic medical records from October 2009 to December 2015 of patients diagnosed with IBD at 10 years of age or younger and prescribed anti-tumor necrosis factor alpha (anti-TNF-α) therapy were reviewed for clinical history, medication history, vaccination history, and hepatitis B and varicella titers. Literature discussing vaccination response in IBD patients were identified through search of the MEDLINE database and reviewed using the key words "inflammatory bowel disease", "immunization", "vaccination", "pneumococcal", "varicella", and "hepatitis B". Non-human and non-English language studies were excluded. Search results were reviewed by authors to select articles that addressed safety and efficacy of immunizations in inflammatory bowel disease. RESULTS: A total of 51 patients diagnosed with IBD prior to the age of 10 and receiving anti-TNF-α therapy were identified. Thirty-three percent of patients (17/51) had incomplete or no documentation of vaccinations. Sixteen case reports, cohort studies, cross-sectional studies, and randomized trials were determined through review of the literature to describe the safety and efficacy of hepatitis B, pneumococcal, and varicella immunizations in adult and pediatric patients with IBD. These studies showed that patients safely tolerated the vaccines without significant adverse effects. Importantly, IBD patients receiving immunosuppressive medications, particularly anti-TNF-α treatment, have decreased vaccine response compared to controls. However, the majority of patients are still able to achieve protective levels of specific antibodies. CONCLUSION: Immunizations have been shown to be well-tolerated and protective immunity can be achieved in patients with IBD requiring immunosuppressive therapy.
Subject(s)
Immunosuppressive Agents/therapeutic use , Irritable Bowel Syndrome/drug therapy , Vaccination/statistics & numerical data , Child , Child, Preschool , Humans , Immunosuppressive Agents/pharmacology , Infant , Retrospective Studies , Tumor Necrosis Factor-alpha/antagonists & inhibitors , VaccinesABSTRACT
BACKGROUND: Rhinovirus (HRV) is associated with the large majority of virus-induced asthma exacerbations in children and young adults, but the mechanisms remain poorly defined. METHODS: Asthmatics and non-asthmatic controls were inoculated with HRV-A16, and nasal epithelial samples were obtained 7 days before, 36 hours after, and 7 days after viral inoculation. RNA was extracted and subjected to RNA-seq analysis. RESULTS: At baseline, 57 genes were differentially expressed between asthmatics and controls, and the asthmatics had decreased expression of viral replication inhibitors and increased expression of genes involved in inflammation. At 36 hours (before the emergence of peak symptoms), 1329 genes were significantly altered from baseline in the asthmatics compared to 62 genes in the controls. At this time point, asthmatics lacked an increase in IL-10 signaling observed in the controls. At 7 days following HRV inoculation, 222 genes were significantly dysregulated in the asthmatics, whereas only 4 genes were dysregulated among controls. At this time point, the controls but not asthmatics demonstrated upregulation of SPINK5. CONCLUSIONS: As judged by the magnitude and persistence of dysregulated genes, asthmatics have a substantially different host response to HRV-A16 infection compared with non-asthmatic controls. Gene expression differences illuminate biologically plausible mechanisms that contribute to a better understanding of the pathogenesis of HRV-induced asthma exacerbations.
Subject(s)
Immunity, Innate , Picornaviridae Infections/immunology , Rhinovirus/pathogenicity , Adult , Asthma/immunology , Case-Control Studies , Female , Humans , Male , Young AdultABSTRACT
Bacteria comprehensively reorganize their global gene expression when faced with starvation. The alarmone ppGpp facilitates this massive response by co-ordinating the downregulation of genes of the translation apparatus, and the induction of biosynthetic genes and the general stress response. Such a large reorientation requires the activities of multiple regulators, yet the regulatory network downstream of ppGpp remains poorly defined. Transcription profiling during isoleucine depletion, which leads to gradual starvation (over > 100 min), allowed us to identify genes that required ppGpp, Lrp and RpoS for their induction and to deduce the regulon response times. Although the Lrp and RpoS regulons required ppGpp for their activation, they were not induced simultaneously. The data suggest that metabolic genes, i.e. those of the Lrp regulon, require only a low level of ppGpp for their induction. In contrast, the RpoS regulon was induced only when high levels of ppGpp accumulated. We tested several predictions of a model that explains how bacteria allocate transcriptional resources between metabolism and stress response by discretely tuning two regulatory circuits to different levels of ppGpp. The emergent regulatory structure insures that stress survival circuits are only triggered if homeostatic metabolic networks fail to compensate for environmental deficiencies.
Subject(s)
Escherichia coli/physiology , Gene Expression Regulation, Bacterial , Guanosine Tetraphosphate/biosynthesis , Bacterial Proteins/metabolism , Escherichia coli/genetics , Escherichia coli/metabolism , Escherichia coli Proteins/metabolism , Gene Expression Profiling , Guanosine Tetraphosphate/genetics , Guanosine Tetraphosphate/metabolism , Isoleucine/metabolism , Leucine-Responsive Regulatory Protein/metabolism , Metabolic Networks and Pathways , Oligonucleotide Array Sequence Analysis , Promoter Regions, Genetic , Regulon , Sigma Factor/metabolism , Stress, PhysiologicalABSTRACT
The stringent response to amino acid starvation, whereby stable RNA synthesis is curtailed in favour of transcription of amino acid biosynthetic genes, is controlled by the alarmone ppGpp. To elucidate the extent of gene expression effected by ppGpp, we designed an experimental system based on starvation for isoleucine, which could be applied to both wild-type Escherichia coli and the multiauxotrophic relA spoT mutant (ppGpp(0)). We used microarrays to profile the response to amino acid starvation in both strains. The wild-type response included induction of the general stress response, downregulation of genes involved in production of macromolecular structures and comprehensive restructuring of metabolic gene expression, but not induction of amino acid biosynthesis genes en masse. This restructuring of metabolism was confirmed using kinetic Biolog assays. These responses were profoundly altered in the ppGpp(0) strain. Furthermore, upon isoleucine starvation, the ppGpp(0) strain exhibited a larger cell size and continued growth, ultimately producing 50% more biomass than the wild-type, despite producing a similar amount of protein. This mutant phenotype correlated with aberrant gene expression in diverse processes, including DNA replication, cell division, and fatty acid and membrane biosynthesis. We present a model that expands and functionally integrates the ppGpp-mediated stringent response to include control of virtually all macromolecular synthesis and intermediary metabolism.