Tunnel of Inflammation in Obstructive Airway Diseases

The use of macrolides for asthma must be put in context of the apparent beneficial affects also observed in complex lung diseases with features of chronic inflammation plus infection such as cystic fibrosis and diffuse panbronchiolitis. It is difficult to determine if this improvement is related to a distinct antiinflammatory property because concurrent bacterial infection or colonization may be present, which has also been implicated in asthma. However, a previous trial12 evaluated the role of clarithromycin in asthma patients that had no evidence of airway colonization with either Mycoplasma pneumoniae or Chlamydia pneumoniae.

In this cohort, clarithromycin treatment decreased BAL fluid IL-12 and tumor necrosis factor-а expression but did not improve in FEV1. In the future, separating the microbial and nonmicrobial properties of the macrolides would assist in determining if the nonmicrobial properties of macrolides could produce the desired antiinflammatory effects in subjects with asthma. Canadian Health and Care Mall treatment your asthma with Canadian medications online. Order asthma medications with 10% discount you can on Canadian Health and Care Mall Shop.

In summary, our results demonstrated that azithromycin possesses antiinflammatory properties in an in vivo noninfectious model of allergic airway inflammation. These observations suggest azithromycin may be beneficial in the treatment of inflammatory conditions, such as asthma, and support the rationale for future prospective randomized clinical trials.

Chronic and persistent airway inflammation is one of the main driving forces in the obstructive airway diseases. It is proving increasingly useful to classify the pattern of inflammation based on the dominant granulocyte present, and there is great potential to use markers of inflammation serially to monitor disease activity and assist in treatment selection and dose adjustment. In asthma, this approach is well developed, particularly for eosinophilic forms of the disease.

The pathway leading to eosinophilic inflammation in asthma is well understood and effectively targeted by treatment. In sensitized individuals, allergen exposure leads to activation of T-helper type 2 lymphocytes, and the resulting cytokine response involving interleukin-5 promotes eosinophilic airway inflammation.


Nasal Allergen Challenge: Systemic Effects

Airway inflammation and remodeling can be present in the lower airways of patients with allergic rhinitis, although it is less intense than in patients with asthma. During natural exposure, both the nose and lung come into contact with airborne allergens. Nasal inflammation may influence lower airway inflammatory processes by the release of inflammatory mediators into the circulation or through an effect on BM progenitors or inflammatory cells.  Nasal Allergen Challenge Systemic Effects

As most clinical trials have been performed during natural allergen exposure, studies evaluating the influence of upper airway disease on lower airways cannot properly assess the influence of nasal inflammation on lower airways. Provocative nasal allergen challenge has been used to help sort out the influences of allergic rhinitis on lower airways and specifically determine the influence of the upper airways on lower airway inflammation. Braunstahl performed nasal allergen provocations in allergic rhinitic patients without asthma and in normal control subjects.

An increase of eosinophils as well as increased expression of intercellular adhesion molecule-1 was observed in the nasal and bronchial biopsies of allergic rhinitic patients compared with control subjects. However, Beeh observed no significant difference in sputum eosinophils following nasal allergen provocation, although sputum ECP and intercellular adhesion molecule were increased. In addition, Braunstahl have shown that segmental bronchial allergen challenge can produce nasal eosinophilic inflammation.

Nasal Allergen Challenge: Systemic Effects

In this regard, we recently performed a study using repeated nasal challenges to determine if this can induce lower airway inflammation and to obtain a more accurate model of allergen exposure. Our preliminary results show that a large number of patients with allergic rhinitis with or without asthma can have significant lower airway inflammation after repeated nasal challenge.

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Hemopoietic Processes as Targets of Therapy

While intranasal steroids can improve lower airway hyperresponsiveness, a greater benefit is seen in patients with both allergic rhinitis and asthma if topical steroids are delivered to both sites of inflam-mation. Of less remarkable but still significant clinical benefit, working through a different pathway, montelukast, a specific leukotriene receptor antagonist (LTRA), has been shown to reduce allergic rhinitis and asthma symptoms. Cysteinyl leuko-trienes (CysLTs) are potent receptor agonist mediators capable of inducing cell recruitment and bronchospasm, increased vascular permeability, and nasal airway resistance. Hemopoietic Processes as Targets of Therapy

Table 1—Effects of Several Antiallergic Treatment Options on Hemopoietic Processes and Eosinophils

Treatment Sputum






Antihistamine Uncertain Reduce/no effect Reduce
LTRA Reduce Reduce Reduce
Topical steroid Reduce Reduce Reduce
Systemic steroid Reduce Reduce Uncertain

Montelukast antagonizes these effects and thus attenuates the allergen-induced early and late asthmatic responses. It also reduces sputum eosinophilia following allergen challenge. Since CysLT receptors are expressed on hemopoietic progenitors, antagonism with montelukast may attenuate tissue eosinophilia via a systemic antiinflammatory effect (see below).

Hemopoietic Processes as Targets of Therapy

Modulation of Eosinophil Differentiation by CS

Hemopoietic mechanisms can be targeted by antiallergic therapies (Table 1). For example, topical treatment with CS can affect the hemopoietic response by abrogation of cytokine production by airways tissues, reduction in peripheral blood Eo/B progenitors, and decreases in BM myeloid progenitors (in a canine asthma model). Most likely, inhaled CS in these models exert their effects on the marrow progenitor response indirectly by interfering with cytokines elaborated from the inflamed tissue, which can then act systemically on the BM. However, a direct effect on progenitors cannot be excluded because there is evidence that, both in vitro and in vivo, low systemic levels of CS (10~9 mol/L) can block differentiation of the Eo/B progenitor in humans and of the myeloid progenitor in dogs.

Road Recovery



To get the most out of the program, we suggest that you take your time. Instead of giving yourself a case of mental suffocation, stop along the way and enjoy what you read. Do the exercises; don’t just think about them. Allow the work to come alive for you, to become part of your life, and to open the way for authentic healing. As you embark on the road to recovery, we suggest that you take note of the next six pointers, which will help prepare you for your journey, imaginal or otherwise.

Six Pointers for Getting Started

  1. Get a notebook (if you haven’t already). Use it to record your dreams and thoughts. This makes it easier to do the work and keep track of your progress. Here, you may write about or draw meaningful or moving experiences you have during any of the exercises or when reading passages in the text.
  2. Write your intentions. Do this on the first page of your notebook. Answer the question: What do I want to get (learn, know, change, heal, find) through using this program? Be as specific as you can. Know that as you go on with the work, your intentions may change. Intentions provide you with a direction. They are not the same as an agenda or goals. And they are not carved in stone.
  3. Record any experiences in your daily life that seem related to this work. This might include events you usually call coincidences; changes in your emotional or physical state; or anything you might perceive differently in yourself or in your relationships with people around you.
  4. Record any night dreams. Write these as soon as possible after you wake up so you don’t forget them, even if they are just fragments that don’t seem important. Dreams are often useful for creating personal imagery for yourself, and they may embody healing messages that our logical, ordinary minds don’t come up with.
  5. Get some blank tapes. Use these to record any of the imagery exercises. Once you are familiar with the exercise, stop using the tape. When you practice the imagery without hearing an outside voice directing you, you begin to become aware of your inner voice.
  6. Be consistent, and do some of this work every day. This might involve practicing an imagery exercise, reading part of the text, writing down a dream, listening to some music, or working with any part of the FUN program that you feel drawn to. Remember, the potency of imaginal medicine depends on your using it, just as you would be expected by your doctor to use your inhaler. Thinking about it won’t do the trick, just as thinking about taking your regular medication would be useless.



Tips on Deciphering the Symptom


What loss am I grieving?

What am I feeling sad about? Who or what am I angry with?


Who or what do I need/want to expel?

Who or what is irritating me?

What or who am I reluctant to give up?

What do I feel pressed to cough up, cough over?

What do I need to confess?


What or who is constricting me?

How am I constricting myself?

What in my life is coming apart?

What am I trying to hold/keep together?


What am I not saying that wants or needs to be said?

Who or what is suffocating me?

Who or what am I not letting go of?


What or who makes me feel choked up?

Who or what is holding me back (how am I feeling choked off)? What or who am I choking on?

What do I need to say?

Pause here and reflect on these questions. Once you have worked with this exercise you may discover some powerful truths regarding your asthma symptoms. However, do not dwell on them. Put them aside and give yourself some space. As you go on, you will acquire more tools for working with these. For now this is enough.


When we refuse to pay attention to our symptoms, we reduce the disease to a meaningless experience. This leaves us stuck in a labyrinth of isolation and despair. To find hope, we learn to live in the here and now and regard our lives as valuable even if not always pleasant. Focusing on our symptoms — really listening to what they have to say — then Undoing our beliefs about our limitations and committing ourselves to Now Act to resolve our difficulties can restore us. “When our focus is toward a principle of relatedness and oneness, and away from fragmentation and isolation, health ensues.”

Rebbe Nachman, the Hasidic teacher, guide, and spiritual master, shared the kind of insight and wisdom that lead to healing our sense of alienation when he said:

If you believe that you can damage, then believe that you can fix.

If you believe that you can harm, then believe that you can heal.

Never despair! Never! It’s forbidden to give up hope.

In the spirit of this advice, the next imagery exercise will help prepare you for what lies ahead.

In the next three chapters you will find specific suggestions, exercises, and healing stories to help integrate FUN into your own life. Important elements of the fun program involve your willingness to:

  • Recognize and separate yourself from the beliefs that have been holding you hostage
  • Listen to the message your symptoms convey to your body-mind
  • Break free of your enslavement to your Committee — those false selves who try to prevent change, even when it heals
  • Ask yourself (and remember to answer), “How am I having FUN in my life?”

article by http://www.healthandcaremall.comcanadian health and care mall.

Canadian Health and Care Mall – What is Diabetes?




Several members of my family developed diabetes when we were young and most of us are controlled by tablets. I’ve been told we are a MODY family. What does this mean?

MODY stands for Maturity-Onset Diabetes of the Young. (Maturity-onset diabetes is an earlier name for Type 2 diabetes.) In the 1970s, it was noticed that a handful of families seemed to develop diabetes in their teens or twenties and about 50% of family members were affected. This suggests a certain sort of inheritance (autosomal dominant); those family members with diabetes have a specific defect in their insulin-producing cells. Research into these patients has increased our understanding of the causes of diabetes. There are several distinct types of MODY, but generally people in this group can control their diabetes with tablets and do not usually need insulin.

If diabetes is known to be in my family, should I or my children take any preventive action?

The inheritance of diabetes is a complicated subject and different types of diabetes are inherited in different ways. In Type 1 diabetes some family members may carry an increased risk, which can be identified by genetic testing.

However, only a small proportion of the people who inherit this risk will go on to develop diabetes and no one has been able to pin down the factors that cause this to happen.

Type 2 diabetes is more strongly inherited than Type 1, and therefore often affects several members of the same family. It is now clear that a number of different genes are involved. The picture which is slowly emerging suggests that there are several different forms of Type 2 diabetes. The genetics of one rare form of inherited diabetes, called MODY, have been investigated in great detail and have increased our understanding of this condition but these discoveries do not apply to the vast majority of people with Type 2 diabetes (see MODY question above).

There is now evidence that family members who are at risk may put off developing diabetes by regular exercise, losing weight and sometimes by taking medication. They should have a blood glucose test as soon as they develop any relevant symptoms, so that diabetes can be detected and treated early.

I am 16 and have had diabetes for five years. Why has my identical twin brother not got diabetes?

A large 20-year research project has studied examples of identical twins with diabetes. The results show a difference between the way Type 1 and Type 2 diabetes are inherited. If you have an identical twin with Type 1 diabetes, you have only a 50% chance of developing diabetes yourself. On the other hand, if you had Type 2 diabetes (extremely unusual at the age of 11) your twin would be almost certain to get the same sort of diabetes. If your twin brother has not developed diabetes within the last five years, he has a very low risk of developing the condition.