Vaccines For Pneumonia, Meningitis Reduce Healthcare Cost Burden

Stopping illnesses through vaccination prevents dying, reduces disease burden and also the investment property through the government to tackle the problem.

Vaccination efforts produced in the earth’s poorest countries since 2001 may have avoided 20 million deaths and saved $350 billion in health-care costs by 2020, according to a different study on the College of New York at Chapel Hill.

‘Vaccinating against hepatitis B, measles, and haemophilus influenzae type b and streptococcus pneumoniae, two bacteria that create pneumonia and meningitis, provided the finest economic benefits.’

Additionally, they place the broader social and economic worth of saving these lives and stopping disabilities at $820 billion.

Researchers brought by Sachiko Ozawa, Ph.D., an affiliate professor in the UNC Eshelman School of Pharmacy, studied the economical impact of Gavi, the worldwide vaccine alliance launched in 2000 to supply vaccines to children within the world’s poorest countries.

Gavi support has led to the immunization of 580 million children, and contains operated mainly within the 73 countries taught in team’s analysis, that was printed within the Bulletin around the globe Health Organization.

“Vaccination is usually considered to become probably the most cost-effective interventions in public places health,” Ozawa stated.

“Decision-makers have to understand the full potential economic benefits that will probably derive from the introduction and sustained utilization of any vaccine or vaccination program.”

Researchers checked out both short- and lengthy-term costs that may be saved stopping illness. The expense – expressed this year U.S. dollars – include averted treatment, transportation costs, productivity losses of caregivers and productivity losses because of disability and dying.

They used the worth-of-a-existence-year approach to estimate the broader social and economic worth of living longer, in better health, because of immunization.

“Our study of the broader social and economic worth of vaccines illustrates the substantial gains connected with vaccination,” she stated.

“Unlike previous estimates that just check out the averted costs of treatment, our estimates from the broader social and economic worth of vaccines reflect the intrinsic value that individuals put on living longer and healthier lives.”

Each one of the Gavi-supported countries within the study may have prevented typically $5 million in treatment costs each year just because of these 10 vaccines. The vaccines may have avoided an believed 20 million deaths, 500 million installments of illness, 9 million installments of lengthy-term disability and 960 million many years of disability by 2020.

The need for preserved productivity, quality of existence along with other broad social and economic benefits for those 73 study countries is believed to achieve $820 billion by 2020, they calculated.

They used health-impact models to estimate the figures of installments of illness, deaths and disability-adjusted existence-years averted by achieving forecasted coverages for vaccination against hepatitis B, human papillomavirus, Japanese encephalitis, measles, rotavirus, rubella, yellow fever and three strains of bacteria that create pneumonia and meningitis.

They discovered that vaccinating against hepatitis B, measles, and haemophilus influenzae type b and streptococcus pneumoniae — two bacteria that create pneumonia and meningitis — provided the finest economic benefits.

Source: Eurekalert

Linoleic acidity metabolite results in steroid resistant bronchial asthma features partly through NF-κB


Rodents grouping

A mans BALB/c rodents (6–8 days) were acquired from Central Drug Research Institute, Lucknow, India and maintained in Institute of Genomics and Integrative Biology (IGIB), Delhi, India. The Institutional Animal Ethical Committee at IGIB approved all rodents experiments and all sorts of methods were performed in compliance using the relevant guidelines and rules of Committee with regards to Control and Supervision of Experiments on Creatures (CPCSEA). Two different allergic models were chosen first being, OVA model with five groups: SHAM (rodents which were PBS sensitized, PBS challenged and given vehicle, 50% ethanol), OVA (rodents which were OVA, grade V chicken egg ovalbumin, sensitized, OVA challenged and given vehicle), OVA + DEX [allergic rodents given dexamethasone (.75 mg/kg) orally], OVA + HODE [allergic rodents administered with intranasal HODE (.6 mg/kg or 2.02 mM) and given vehicle] and OVA + HODE + DEX [allergic rodents administered with intranasal HODE (.6 mg/kg or 2.02 mM) and given dexamethasone (.75 mg/kg) orally]. The 2nd model had following groups: SHAM, OVA, OVA + DEX, OVA + HODE + DEX, and OVA + HODE + DEX + PDTC [OVA + HODE + DEX rodents administered with PDTC dissolved in DMSO (50 mg/kg) intra-peritoneally].

OVA-immunization and challenge

Rodents were sensitized with three intraperitoneal injections of 50 µg OVA adsorbed in alum for 3 days and challenged with 3% OVA in PBS for seven days as described earlier21, 46, 47.

Administration of 13-S-HODE, Dexamethasone, and PDTC

13-S-HODE (Cayman, Michigan,USA) or VEH (50% ethanol) was instilled towards the nasal openings of every isoflurane anesthetized mouse. According to our previous publication21 we’ve selected the dose of .6 mg/kg or 2.02 mM for every mouse. 13-S-HODE was administered intranasally on days 24, 26 and 28 as proven in Fig. 1A. Dexamethasone (Sigma-Aldrich, MO, USA), dissolved in 50% ethanol, was handed orally (.75 mg/kg) to rodents from day 24 to twenty-eight as proven in Fig. 1A. PDTC (Sigma-Aldrich, USA) was dissolved in DNAase and RNAase free H2O, and it was administered intraperitoneally into mouse (50 mg/kg) on days 24, 26 and 28, 2 hrs following the administration of HODE (Figs 1A and 5A).

Airway hyperresponsiveness measurement and bronchoalveolar lavage (BAL)

Airway hyper-responsiveness was believed with invasive flexiVent (SCIREQ, Montreal, Canada) as formerly described21, 46, 47. BAL was performed and differential cell counts were created as described earlier21, 46, 47.

Lung histopathology

Formalin-fixed lung sections were stained with Haematoxylin & Eosin (H & E), Periodic acidity-Schiff and morphometric analysis was performed using openly available Image J software21, 46, 47.

In vitro experiments

Human bronchial epithelial cells (Beas-2B) were acquired (ATCC, Manassas, Veterans administration, USA), maintained in HAM’s F12 (Sigma-Aldrich, MO, USA) with 10% fetal bovine serum (FBS). Cells were pretreated with dexamethasone (10−6 M, Sigma, MO, USA) for 3 hrs before stimulating with vehicle (ethanol) or 13-S-HODE (35 μM, Cayman, Ann Arbor, Michigan, USA) for 16 hrs. These cells were harvested for more experiments and supernatants were stored for cytokine assays.

ELISAs

IL-8, MCP1-α (E-biosciences, CA, USA), myeloperoxidase assay (Cayman chemicals, Michigan, USA) were performed based on manufacturer’s instructions from culture supernatants (IL-8, MCP1-α) and BAL Fluid correspondingly.

For calculating GR activity (Active Motif, CA, USA) BEAS-2B cells acquired after HODE and DEX treatment (as described above), were processed for nuclear extract. Elisa was performed using manufacturer’s protocol with 20 μg of nuclear extract. The O.D measured is plotted in arbitrary units (AU) in fold change, calculated by O.D test/O.D veh48.

Immunohistochemistry

Immunohistochemical analysis for p-NFkB and IkB-α (Santa Cruz Biotechnology, Texas, USA) was performed with particular secondary antibodies (Sigma, St. Louis, MO, USA).

Real-time PCR

Cells harvested were lysed in RNA lysis solution and RNA was isolated (Qiagen, Germany). cDNA was isolated from RNA while using manufacture’s protocol (ABI, CA, USA). Further real-time was performed using kappa FAST Syber eco-friendly (Roche cycler) while using following primers. Human GR-α, FP: 5′ACGGTCTGAAGAGCCAAGAG3′and RP: 5′CAGCTAACATCTCGGGGAAT3′ Human β-actin, FP: 5′CCAACCGCGAGAAGATGA3′, RP: 5′ CCAGAGGCGTACAGGGATAG3′.

Record analysis

All data represents mean ± SEM n = 3–6 each group *p < 0.05, **p < 0.01, ***p < 0.001. A p-value more than 0.05 is considered non-significant (NS). Statistical significance of the differences between paired groups was determined with a two-tailed Student’s t test. One-way analysis of variance was utilized to check multiple groups by utilizing PRISM software and it was evaluated further having a nonparametric Mann-Whitney rank-sum test or Krusker-wallis test wherever appropriate.

Research findings might be start of new possible strategy to Parkinson´s disease

Parkinson´s disease is really a chronic disease with unknown causes. The condition destroys the mind cells that control body movements. Shivering, stiff legs and arms and poor coordination are normal signs and symptoms of Parkinson’s. The signs and symptoms may develop gradually, also it sometimes needs time to work to create a correct diagnosis.

Researchers in the Department of worldwide Public Health insurance and Primary Care (IGS) in the College of Bergen (UiB) have finished a sizable study that incorporated data in the Norwegian Prescription Database, in cooperation with researchers at Harvard College.

“Our analysis of information in the whole Norwegian population continues to be decisive for that conclusion within this study,” states Professor Trond Riise at IGS. He leads the registry study in Norwegian.

100 million prescriptions

Along with colleagues Anders Engeland and Kjetil Bjørnevik, Riise has examined greater than 100 million Norwegian prescriptions registered since 2004.

Within the study, treating Parkinson’s was associated with prescriptions of bronchial asthma medicine and also the medicine for top bloodstream pressure. It enabled they to determine the bond between medicine use and illness.

The UiB-researchers could make these comparisons using the prescription database. The Norwegian analysis ended after researchers at Harvard College found these results of the medicines in animal tests as well as in experiments with cognitive abilities within the lab. Their results demonstrated these different medicines had opposite effects on the chance of Parkinson’s.

Possible new treatment

To determine if these medicines had exactly the same impact on humans, they at Harvard College began to collaborate using the Norwegian research team, as well as their unique resource of getting accessibility unique and enormous Norwegian database, where all Norwegian prescriptions are registered.

“We examined the entire Norwegian population and located exactly the same results as with your pet testing at Harvard College. These medicines haven’t been studied with regards to Parkinson’s disease,” states Riise.

Trond Riise underlines the truth that “Our breakthroughs could be the oncoming of an entirely new possible strategy to this serious disease. We predict that studies follows these breakthroughs.”

Source:

http://world wide web.uib.no/en/mediterranean/110169/bronchial asthma-medicine-halves-risk-parkinson%C2%B4s

Ragweed Woes: How you can Win Against Certainly one of Pollen’s Worst Offenders

Say “ragweed” inside a crowded room and you’re certain to hear some groans. Why? Because ragweed is easily the most common weed pollen allergy, affecting 10-20 percent of american citizens.

For those who have a ragweed pollen allergy, you might curently have “hay fever” signs and symptoms. Ragweed pollen season peaks in August and September in many areas of the U . s . States, particularly in Eastern and Midwestern states.

Hay fever is also referred to as periodic allergic rhinitis. Signs and symptoms include:

  • Itching within the nose and eyes
  • Sneezing
  • Stuffy nose (congestion)
  • Runny nose
  • Mucus (phlegm) within the throat (postnasal drip)

Ragweed pollen can be difficult to flee from. One good reason why ragweed pollen creates a lot of issues for individuals with bronchial asthma and allergic reactions happens because one plant can establish as much as 1 billion pollen grains. That’s lots of pollen!

Ragweed pollen also travels far. Even though you don’t reside in a province where ragweed will probably grow, you may still have it. Ragweed pollen has been discovered so far as 400 miles to ocean and a pair of miles up in mid-air.

Ragweed pollen includes a major effect on individuals with pollen allergic reactions and allergic bronchial asthma. While it’s difficult to avoid completely, there are methods you are able to win from this pressure of nature.

The easiest way you are able to fight ragweed pollen is as simple as preparing prior to the season begins. Discover when ragweed months are in your town and begin following through before it also starts.

  • Visit a board-certified allergist. They are able to confirm your allergy which help generate cure intend to manage your signs and symptoms.
  • Watch pollen counts. Within the late summer time, track the pollen in your town so that you can know when ragweed begins to rise. You will get your area’s pollen counts from the National Allergy Bureau.
  • Schedule your time and effort outdoors before 10 a.m. after 3 p.m. Ragweed pollen amounts peak in the center of your day.
  • Use central heat and air and doorways and home windows closed.
  • Shower and shampoo hair every evening before going to sleep to help keep pollen from getting into the bedding.
  • Stick to your plan for treatment. Make certain you do not miss any doses of the medicines.

Medical Review August 2017.

You should stay awake-to-date on news about bronchial asthma and allergic reactions. By joining our community and following our blog, you will get news about research and coverings. Our community offers an chance for connecting along with other patients who manage these conditions for support.

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How to prevent Allergy and Bronchial asthma Triggers During Outside Holiday Celebrations

Outside occasions, cookouts and picnics are smart ways to get along with family and buddies to celebrate. For those who have allergic reactions and asthma, be familiar with possible triggers and allergens surrounding you and do something to avoid flare-ups.

1. Smoke from Barbecues or Fire Bowls

Smoke from fires for example barbecues, bonfires or fire bowls may also trigger bronchial asthma. If you’re hosting the party, consider cooking inside. If you’re attending another person’s party, attempt to avoid the road to smoke. 

2. Insects

Insects are unwelcome visitors at most outside celebrations. They are not only annoying, but they may also cause serious trouble for individuals with insect allergic reactions, especially to stinging insects. For many, they are able to result in a existence-threatening allergic attack known as anaphylaxis (anna-fih-LACK-sis).

Probably the most common stinging insects that create allergy symptoms are bees, wasps, hornets, yellow jackets and fire ants. Many people have severe reactions to biting insects like nasty flying bugs. If you realize you’ve severe reactions to insect bites or stings, make sure to carry your epinephrine auto-injectors along with you whatsoever occasions.

3. Pollen

The top pollen in lots of areas throughout the summer time is grass pollen. In northern parts of the U . s . States, grasses usually pollinate within the late spring or early summer time. In southern regions, grasses may pollinate throughout many seasons and may trigger signs and symptoms all year round. Follow our ten tips for managing grass pollen allergy.

Throughout the late summer time and early fall, ragweed pollen causes problems. If you are celebrating when ragweed is high, follow our recommendation on coping with ragweed pollen.

4. Scents

Scented products also lead to polluting of the environment and may trigger bronchial asthma. You might encounter:

  • scented candle lights (like individuals to accustomed to repel bugs outdoors)
  • scented oil in tiki torches
  • strong perfume or perfume on other visitors
  • odor-hiding fragrances and air fresheners

If scents trigger your bronchial asthma, you may want to send a polite request towards the host prior to the party to inquire about they not use these kinds of products. It isn’t an enjoyable celebration for anybody if your guest encounters breathing distress throughout a party.

5. Fireworks

Fireworks are aren’t only for the 4th of This summer any longer. They’ve end up part of many holiday celebrations. But fireworks create smoke and small particulate matter that includes to air pollution which can trigger bronchial asthma. Consider watching fireworks from the inside.

AAFA wishes a happy and safe celebration!

Cesarean section without medical indication and perils of childhood allergic disorder, attenuated by breastfeeding

Our study implies that CS without medical indication is connected with elevated perils of childhood bronchial asthma and allergic rhinitis. CS for fetal complications can also be connected by having an elevated chance of allergic rhinitis in youngsters. This outcome is in line with previous studies generally3, 14, 15. Breastfeeding may attenuate these risks.

Inside a recent population-based data-linkage study of 321,287 term singleton first-born offspring in Scotland, Uk, Black et al.14 discovered that in comparison to children born vaginally, offspring born by planned CS were in an elevated chance of bronchial asthma requiring hospital admission (adjusted hazard ratio = 1.22 [95% CI, 1.11–1.34]) and salbutamol inhaler prescription at five years (adjusted hazard ratio = 1.13 [95% CI, 1.01–1.26]). This finding is in line with what meta-analysis, by which CS was connected having a 20% rise in the chance of bronchial asthma3.

It’s been an issue in the past studies the association between CS and bronchial asthma are closely related to confounding by indication because most CS in individuals studies were performed for clinical indications. Our studies are the initial to particularly check out the association in CS without medical indication. The findings were in line with previous investigations generally. Even though the exact underlying biological mechanism is unclear, it’s been hypothesized that fetuses delivered by CS mostly are uncovered to microflora that’s predominately on maternal skin after birth, although not in maternal vagina16. The microbial types and colonization in youngsters delivered by CS can lead to an altered gut microbiota at the begining of existence, which might impair natural growth and development of defense mechanisms after which promote the introduction of immune-mediated bronchial asthma and allergic disorders16. Preliminary evidence shows that by hand exposing newborns delivered by CS to maternal vaginal microbes may partly restore the microbiota of those infants17. The protective aftereffect of exclusive breastfeeding around the perils of bronchial asthma and allergic rhinitis because of CS within our study, may make sure microflora-related mechanism, thinking about that breastfeeding could prevent allergy through controlling infant gut barrier function and microbiota18.

Nevertheless, our studies cannot directly prove a causal relationship. Indeed, a brother or sister analysis using Swedish medical registry data unsuccessful to verify the association between CS and childhood bronchial asthma19. However, if gut microflora dysbiosis is causally associated with childhood bronchial asthma, it’s reasonable to wonder if the matched brother or sister design may mask the outcome of mode of delivery since the microbial exposure continues after birth. Numerous research has proven that close connection with older brothers and sisters and pets may prevent bronchial asthma7,8,9. In Shanghai, China, because of the one-child-family policy, the majority of our study subjects were single child20, and couple of families have pets in your own home.

Several limitations in our research is important to note. First, info on CS and it is indications were self-reported. An earlier study shown the precision of maternal recall of CS 3 to nine years ago was 100%, and maternal recall of severe obstetric complications seemed to be rather reliable21. Furthermore, the prevalence of CS within our study was 47%, that was in conjuction with the previous survey in Shanghai (48%)22. The speed of CS without medical indications (18%) within our study can also be much like that inside a previous report in which the rate of CS on maternal request was 20%11. Therefore, the self-reported CS and it is indications might be reasonably accurate within our study.

Second, bronchial asthma and allergic rhinitis within the index children were also as reported by the mother and father. Thus, inaccuracy within the result’s possible. Within our study, the prevalence of bronchial asthma was 3.4%, that is less than 5.81–7.57% reported in the past studies from Shanghai23, 24. However the prevalence of allergic rhinitis within our study (15%) was in line with an earlier report (13%)25. Discrepancy in bronchial asthma prevalence might be partially because of the incompatibility in our study population and also the previous ones. Within our population-based study, we at random selected subjects all 17 districts and counties and incorporated individuals from suburb and rural areas in Shanghai, whereas the prior studies only selected children from cities23, 24. Since bronchial asthma prevalence in youngsters of province in Shanghai is gloomier than individuals in urban area (3.7% versus. 6.2%)26, the low prevalence of childhood bronchial asthma within our study might be partly expected.

However, the underestimation of bronchial asthma prevalence can’t be completely eliminated, which can be because of underreporting through the parents. It’s possible that some parents might not want the college be aware of child history because this survey was conducted with the school, despite the fact that we ensured the mother and father within the informed consent the information they provided could be strictly private. So we were not able to ensure the self-report. However, we purposefully placed the questions about CS history far aside from individuals on child disease history within the questionnaire. Thus, we speculate the misclassification from the connection between interest was less inclined to be differential. We further controlled for maternal and paternal education and family earnings within the analysis.

Third, the information on feeding in infancy was remembered by parents. Within our study, the prevalence of exclusive breastfeeding looked like that formerly reported in Shanghai, around 50%27. Thus, this recall might not be seriously biased.

Finally, our study didn’t collect data on genealogy of allergic disorders. Previous study discovered that kids with genealogy of allergy were built with a greater chance of bronchial asthma than individuals without genealogy28. Since genealogy of bronchial asthma isn’t related to CS, it might not confound the association between CS and also the perils of childhood bronchial asthma and allergic rhinitis.

Can Antibacterial Drug Combination Combat Drug-Resistant T . b?

Mixing the antibiotic ceftazidime using the enzyme inhibitor avibactum happens to be an effective strategy to drug-resistant t . b, reveals new research.

This antibacterial drug combination already in clinical use for Gram-negative microbial infections could help with stemming the growing global drug-resistant t . b crisis. Mycobacterium t . b (or Mtb) causes among the world’s deadliest illnesses.

‘Combination of Ceftazidime-avibactam (CAV) might be a safer choice for women that are pregnant and Aids-infected patients. ’

Based on the World Health Organization, 10.4 million people contracted Mtb and 1.8 million died in the disease in 2015. While newer antibiotics like bedaquiline and delamanid have improved patient outcomes, they’re still connected having a 24-month treatment failure rate of 38% in individuals with extensively drug-resistant Mtb.
Hunting for a much-needed road to immediately deploy new treatments (when compared to frequently decade-lengthy road to approval that many experimental agents under analysis face), Deyvani Deshpande and colleagues examined the unexploited Mtb-fighting potential of presently marketed compounds. They studied commercially accessible CAV (a duo of ceftazidime and avibactam) and compared its usefulness with other first-line regimens utilizing a screening tool endorsed through the Food and drug administration (known as the hollow fiber system model, which enables for any quick study of drug effectiveness according to human lung pharmacokinetics).

With computer-aided simulations, they identified optimal CAV doses according to bodyweight in grown-ups and youthful children. Deshpande et al. state that CAV might be a safer choice for women that are pregnant and Aids-infected patients, which numerous studies are the next phase to check the drug combination.

The authors’ approach could be employed to accelerate the identification of other promising antibiotic candidates in several weeks instead of years.

Source: Eurekalert

Breastfeeding may safeguard children from bronchial asthma exacerbations later in existence

Inside a Pediatric Allergy and Immunology analysis of kids with bronchial asthma, individuals who was simply breastfed were built with a 45% lower chance of bronchial asthma exacerbations later in existence in contrast to children who was not breastfed.

Investigators examined data from 960 children aged 4 to 12 years who have been using regular bronchial asthma medication.

“Although within our study breastfeeding was proven to become a protective factor for bronchial asthma exacerbations, it’s still unclear whether there’s a causal relation between breastfeeding and bronchial asthma exacerbations nevertheless the relation may be described through the influence of breastfeeding around the defense mechanisms. Alterations in the composition and activity from the gut microbiome at the begining of existence may influence the defense mechanisms which changes might not directly result in alterations in bronchial asthma later in existence,” stated Dr. Anke Maitland-van der Zee, senior author from the study. “Further prospective scientific studies are warranted to verify this association and also to clarify the actual mechanisms.”

Source:

http://newsroom.wiley.com/press-release/pediatric-allergy-and-immunology/breastfeeding-may-help-prevent-childrens-bronchial asthma-exace

Individuals With Bronchial asthma and Allergic reactions Have to take Safeguards During Cleanup Following a Ton

Following a natural disaster with flooding, individuals with bronchial asthma and allergic reactions have to take extra safeguards because they begin cleanup efforts. Lengthy after waters have receded, ton waters can bid farewell to chemicals, bacteria, infections and mold. These may create lengthy-term health problems for those who have bronchial asthma and allergic reactions.

Mold is among the greatest concerns following a ton. Mold, a fungus, can grow in almost any moist atmosphere. It differs from plants or creatures in the way it reproduces and grows. The “seeds,” known as spores, traverse the environment. Mold spores enter into onto your nose and cause allergy signs and symptoms. They can also achieve your lung area and trigger bronchial asthma.

In case your home continues to be flooded or has water damage and mold, mold may begin growing that you don’t expect. It doesn’t disappear because the water dries. Mold may grow inside furniture or under carpet that got wet, which makes it difficult to find. Otherwise replaced, it will make your family very sick. Products which have become wet from the ton need to be completely cleaned and dried or discarded.

Use these tips to avoid lengthy-term signs and symptoms from mold:

  • Put on a mask to safeguard yourself whenever you return to your house.
  • Consider getting a professional to complete the cleanup.
  • Get rid of furniture along with other products that can’t be cleaned immediately.
  • Create ventilation in your house by opening home windows and taking advantage of an authorized bronchial asthma &amp allergy friendly air cleanser.
  • If at all possible, find another destination before the mold continues to be cleared up.

There are lots of health issues to consider when clearing up mold following a ton. Browse the Homeowner’s and Renter’s Guide to Mold Cleanup After Disasters from the Ecological Protection Agency for additional tips and precautions. 

Houston and surroundings areas continue to be within an active ton zone. Lots of people are displaced by Hurricane Harvey and won’t be able to come back home for a while. Individuals with bronchial asthma and food allergic reactions have limited use of necessary medical equipment and safe food. Read our blog to discover the best way to help. 

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Relationship between fraction of exhaled nitric oxide supplement and airway morphology assessed by three-dimensional CT analysis in bronchial asthma

  • 1.

    Global Initiative for Bronchial asthma. Global Technique for Bronchial asthma Management and Prevention, 2017. http://world wide web.ginasthma.org (2017)

  • 2.

    Gupta, S. et al. Quantitative analysis of high-resolution computed tomography scans in severe bronchial asthma subphenotypes. Thorax 65, 775–781 (2010).

  • 3.

    Hartley, R. A. et al. Relationship between breathing and quantitative computed tomographic parameters of airway remodeling, air trapping, and emphysema in patients with bronchial asthma and chronic obstructive lung disease: Just one-center study. J. Allergy Clin. Immunol. 137, 1413–1422.e12 (2016).

  • 4.

    James, A. L., Paré, P. D. & Hogg, J. C. The mechanics of airway narrowing in bronchial asthma. Am. Rev. Respir. Dis. 139, 242–246 (1989).

  • 5.

    Kuwano, K. et al. Small airways dimensions in bronchial asthma as well as in chronic obstructive lung disease. Am. Rev. Respir. Dis. 148, 1220–1225 (1993).

  • 6.

    Aikawa, T., Shimura, S., Sasaki, H., Ebina, M. & Takishima, T. Marked cup cell hyperplasia with mucus accumulation within the airways of patients who died of severe acute bronchial asthma attack. Chest 101, 916 (1992).

  • 7.

    Hamid, Q. et al. Inflammation of small airways in bronchial asthma of small airways in bronchial asthma. J. Allergy Clin. Immunol. 100, 44–51 (1997).

  • 8.

    Roche, W., Johnson, J., Beasley, R. & Holgate, S. Subepithelial fibrosis within the bronchi of asthmatics. Lancet 333, 520–524 (1989).

  • 9.

    Bai, T. R., Cooper, J., Koelmeyer, T., Pare, P. D. & Weir, T. D. The result old and time period of disease on airway structure in fatal bronchial asthma. Am. J. Respir. Crit. Care Mediterranean. 162, 663–669 (2000).

  • 10.

    Boulet, L. P. et al. Bronchial subepithelial fibrosis correlates with airway responsiveness to methacholine. Chest 112, 45–52 (1997).

  • 11.

    Chetta, A. et al. Bronchial responsiveness to sterilized water and methacholine and it is relationship to inflammation and remodeling from the airways In bronchial asthma. Am J Respir Crit Care Mediterranean 153, 910–7 (1996).

  • 12.

    Nakano, Y. et al. Computed tomographic measurements of airway dimensions and emphysema in smokers correlation with breathing. Am. J. Respir. Crit. Care Mediterranean. 162, 1102–1108 (2000).

  • 13.

    Berger, P. et al. Airway wall thickness in smokers: quantitative thin-section CT assessment. Radiology 235, 1055–1064 (2005).

  • 14.

    Aziz, Z. A. et al. Functional impairment in emphysema: Contribution of airway abnormalities and distribution of parenchymal disease. Am. J. Roentgenol. 185, 1509–1515 (2005).

  • 15.

    Hasegawa, M. et al. Air flow limitation and airway dimensions in chronic obstructive lung disease. Am. J. Respir. Crit. Care Mediterranean. 173, 1309–1315 (2006).

  • 16.

    Coxson, H. O. et al. Airway wall thickness assessed using computed tomography and optical coherence tomography. Am. J. Respir. Crit. Care Mediterranean. 177, 1201–1206 (2008).

  • 17.

    Hasegawa, M. et al. Relationship between improved air flow limitation and alterations in airway calibre caused by inhaled anticholinergic agents in Chronic obstructive pulmonary disease. Thorax 64, 332–338 (2009).

  • 18.

    Inui, N. et al. Results of indacaterol versus tiotropium on respiratory system mechanics assessed through the forced oscillation technique in patients with chronic obstructive lung disease. Int. J. Chronic obstructive pulmonary disease 10, 1139–1146 (2015).

  • 19.

    Yasui, H. et al. Multidetector-row computed tomography assessment of adding budesonide/formoterol to tiotropium in patients with chronic obstructive lung disease. Pulm. Pharmacol. Ther. 26, 336–41 (2013).

  • 20.

    Karayama, M. et al. Respiratory system impedance is correlated with morphological alterations in the lung area on three-dimensional CT in patients with Chronic obstructive pulmonary disease. Sci. Repetition. 7, 41709 (2017).

  • 21.

    Niimi, A. et al. Airway wall thickness in bronchial asthma assessed by computed tomography: Regards to clinical indices. Am. J. Respir. Crit. Care Mediterranean. 162, 1518–1523 (2000).

  • 22.

    Niimi, A. et al. Relationship of airway wall thickness to airway sensitivity and airway reactivity in bronchial asthma. Am. J. Respir. Crit. Care Mediterranean. 168, 983–988 (2003).

  • 23.

    Awadh, N., Müller, N. L., Park, C. S., Abboud, R. T. & Fitzgerald, J. M. Airway wall thickness in patients with near fatal bronchial asthma and control groups: assessment rich in resolution computed tomographic checking. 248–253 (1998).

  • 24.

    Marchac, V. et al. Thoracic CT in pediatric patients with difficult-to-treat bronchial asthma. Am. J. Roentgenol. 179, 1245–1252 (2002).

  • 25.

    Siddiqui, S. et al. Airway wall geometry in bronchial asthma and nonasthmatic eosinophilic bronchitis. Allergy 64, 951–958 (2009).

  • 26.

    Lee, Y. et al. High-resolution CT findings in patients with near-fatal bronchial asthma: comparison of patients with mild-to-severe bronchial asthma and normal control subjects and alterations in airway abnormalities following steroid treatment. Chest 126, 1840–1848 (2004).

  • 27.

    Aysola, R. S. et al. Airway remodeling measured by multidetector CT is elevated in severe bronchial asthma and correlates with pathology. Chest 134, 1183–1191 (2008).

  • 28.

    Kurashima, K. et al. Aftereffect of early versus late intervention with inhaled corticosteroids on airway wall thickness in patients with bronchial asthma. Respirology 13, 1008–13 (2008).

  • 29.

    de Blic, J. et al. High-resolution computed tomography scan and airway remodeling in youngsters with severe bronchial asthma. J. Allergy Clin. Immunol. 116, 750–754 (2005).

  • 30.

    Kasahara, K., Shiba, K., Ozawa, T., Okuda, K. & Adachi, M. Correlation between your bronchial subepithelial layer and whole airway wall thickness in patients with bronchial asthma. Thorax 57, 242–246 (2002).

  • 31.

    Hamid, Q. et al. Induction of nitric oxide supplement synthase in bronchial asthma. Lancet 342, 1510–3 (1993).

  • 32.

    Payne, D. N. R. et al. Relationship between exhaled nitric oxide supplement and mucosal eosinophilic inflammation in youngsters with difficult bronchial asthma, after treatment with dental prednisolone. Am. J. Respir. Crit. Care Mediterranean. 164, 1376–1381 (2001).

  • 33.

    Warke, T. J. et al. Exhaled nitric oxide supplement correlates with airway eosinophils in early childhood bronchial asthma. Thorax 57, 383–387 (2002).

  • 34.

    Lehtimäki, L., Kankaanranta, H., Saarelainen, S., Turjanmaa, V. & Moilanen, E. Elevated alveolar nitric oxide supplement concentration in asthmatic patients with nocturnal signs and symptoms. Eur. Respir. J. 20, 841–845 (2002).

  • 35.

    Scichilone, N. et al. Alveolar nitric oxide supplement and bronchial asthma control in mild untreated bronchial asthma. J. Allergy Clin. Immunol. 131, 1513–1517 (2013).

  • 36.

    van Veen, I. H. et al. Alveolar nitric oxide supplement versus measures of peripheral airway disorder in severe bronchial asthma. Eur. Respir. J. 27, 951–956 (2006).

  • 37.

    Mahut, B. et al. Both inflammation and remodeling influence nitric oxide supplement output in youngsters with refractory bronchial asthma. J. Allergy Clin. Immunol. 113, 252–256 (2004).

  • 38.

    Powell, H. et al. Control over bronchial asthma during pregnancy led by measurement of fraction of exhaled nitric oxide supplement: a dual-blind, randomised controlled trial. Lancet 378, 983–990 (2011).

  • 39.

    Andrew, D. S., Cowan, J. O., Brassett, K. P., Herbison, G. P. & Taylor, D. R. Utilization of exhaled nitric oxide supplement measurements to steer treatment in chronic bronchial asthma. New Engl J Mediterranean 352, 2163–2173 (2005).

  • 40.

    Hughes, J. M. et al. Human eosinophil-airway smooth muscle cell interactions. Mediators Inflamm. 9, 93–9 (2000).

  • 41.

    Januskevicius, A. et al. Eosinophils enhance WNT-5a and TGF-β1 genes expression in airway smooth muscle tissues and promote their proliferation by elevated extracellular matrix proteins production in bronchial asthma. BMC Pulm. Mediterranean. 16, 94 (2016).

  • 42.

    Januskevicius, A. et al. Suppression of eosinophil integrins prevents remodeling of airway smooth muscle in bronchial asthma. Front. Physiol. 7, 1–13 (2017).

  • 43.

    Hyde, R. W. et al. Resolution of manufacture of nitric oxide supplement by lower airways of humans-theory. J Appl Physiol 82, 1290–1296 (1997).

  • 44.

    Lehtimäki, L., Kankaanranta, H., Saarelainen, S., Hahtola, P. & Järvenpää, R. Extended exhaled NO measurement differentiates between alveolar and bronchial inflammation. Am J Respir Crit Care Mediterranean 163, 1557–1561 (2001).

  • 45.

    Niimi, A. et al. Aftereffect of short-term treatment with inhaled corticosteroid on airway wall thickening in bronchial asthma. Am. J. Mediterranean. 116, 725–731 (2004).

  • 46.

    Mummadi, S. R. & Hahn, P. Y. Update on exhaled nitric oxide supplement in clinical practice. Chest 149, 1340–1344 (2016).

  • 47.

    Gelb, A. F. et al. Elevated nitric oxide supplement concentrations within the small airway of older normal subjects. Chest 139, 368–375 (2011).

  • 48.

    Tsoukias, N. M. & George, S. C. A 2-compartment type of lung nitric oxide supplement exchange dynamics. J. Appl. Physiol. 85, 653–66 (1998).

  • 49.

    Capraz, F., Kunter, E., Cermik, H., Ilvan, A. & Pocan, S. The result of inhaled budesonide and formoterol on bronchial remodeling and HRCT features in youthful asthmatics. Lung 185, 89–96 (2007).

  • 50.

    Inoue, T., Kitamura, Y., Li, Y. & Ito, W. Robust airway extraction according to machine learning and minimum spanning tree. Proceeding SPIE 8670, 86700L (2013).

  • 51.

    American Thoracic Society. ATS/ERS strategies for standardized procedures for that offline and online measurement of exhaled lower respiratory system nitric oxide supplement and nasal nitric oxide supplement, 2005. Am. J. Respir. Crit. Care Mediterranean. 171, 912–930 (2005).

  • 52.

    Japanese Respiratory system Society. Guidelines of respiratory system function tests: spirometry, flow-volume curve, and diffusion capacity from the lung. Tokyo, japan Japanese Respir. Soc (2004).

  • 53.

    Diedenhofen, B. & Musch, J. Cocor: an extensive solution for that record comparison of correlations. PLoS One 10, e0121945 (2015).

  • 54.

    Diedenhofen, B. & Musch, J. cocor: Evaluating Correlations. Version 1.1-3. https://cran.r-project.org/package=cocor (2015).

  • 55.

    Revelle, W. psych: Procedures for Personality and Mental Research. Version = 1.7.3 https://CRAN.R-project.org/package=psych (2017).