Manual Colby the Coal Mining Bee

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Contents:
  1. Fold A Flame, portable fire pits that pack flat
  2. Five fun fact-filled days out
  3. More on this...
  4. colby the coal mining bee Manual
  5. 1. Introduction

Activities include making fire, building shelter, finding water, wildlife awareness, animal tracking, nature walks and archery. Whether you fancy a family outing, or a great experience for a group of children, there are a number of choices available. Buzzard Chris Bushcraft is in South Pembrokeshire, and offers a range of different courses.

Some organisations can also take you for a meal from the outdoors.

Fold A Flame, portable fire pits that pack flat

With wild food foraging, your children can find fresh food and herbs from a variety of places, as well as learning how to prepare and cook them. Funghi Forays are based in the Elan Valley and offer a chance to learn about the wild mushrooms available out there. Wild About Pembrokeshire can take you out foraging along the seashore or down hedgerows, to learn about what to eat and how to cook it.

Wild Pickings is based in Cardigan and runs courses which children can join too.

Coal In Kentucky (Full Documentary)

Why not come for an educational yet tasty experience! Set in the beautiful Ceredigion countryside across which their hives are spread, New Quay Honey Farm combines an informative day out with the opportunity to treat your family. Learn how bees live, hives work and honey is produced, or search for the queen bee and watch her lay her eggs. Also learn about their tropical ant colony. The farm produces a range of honey, including set or runny, heather, mountain or wildflower.

Five fun fact-filled days out

It also has a Meadery where its own honey is turned into mead with several flavours available, and where you can learn about the process and the history of Welsh mead, the oldest known alcoholic drink. The Tearoom serves homemade cakes, cream teas and ice creams, including honey flavoured ice cream! There is also a Wildlife Garden, Picnic Area, Visitor Centre and Shop, selling their honey, mead, and beeswax products such as candles, cosmetics and polish.

There are also exhibitions and courses available including Beekeeping and Cookery Courses. Also visit: Brynderi Honey Farm for homemade ice creams and sorbets; C aws Cenarth Creamery for delicious local cheeses and how they are made. Stay at: Penyrallt Cottage ; Fronnant , or one of the other lovely cottages in the Cardigan Bay area. For information and prices visit the New Quay Honey Farm website or call Come for an adventure in the great outdoors where you can meet the wildlife up close.

Llanelli Wetlands Centre has a great assortment of ducks, swans and geese to meet — and feed by hand! There are exotic Caribbean Flamingos, Butterflies, Dragonflies, as well as a host of other birds and wildlife to spot around the site — and with recent sightings posted to let you know what to look out for. With acres of wildlife-packed wetlands to explore, complete with paths, Nature Trails and Viewing Tower, your children will learn a lot and play a lot! There are a range of hides to watch birds and wildlife from, with views of marshland and the estuary. There are seasonal activities during the holidays or at weekends — build a den, try pond-dipping or a variety of indoor crafts.

Open 9. Stay at: Trepartridge Cottage or another one of our Carmarthenshire cottages. Enter your email address to subscribe to this blog and receive notifications of new posts by email. Email Address. The Real Wales. Skip to content. Although tobacco smoking is the most common cause of emphysema and chronic obstructive pulmonary disease COPD , various other types of lung injury have been described due to smoke exposure and are encompassed within the ILD spectrum of disease [ 44 , 45 , 46 ].

The precise amount of smoke exposure required to cause the various forms of ILD is unknown, but is generally thought to occur in a dose-dependent fashion [ 47 , 48 ]. A detailed history regarding the use and quantity of cigarettes, electronic cigarettes, marijuana, or other illicit substances in conjunction with chest CT imaging patterns will indicate smoking-related ILD as the most likely specific process. RB and DIP are usually considered spectrums of the same disease process [ 1 , 2 , 49 ] and are defined based on radiographic and histopathologic findings.

Both disorders demonstrate the abnormal accumulation of finely pigmented alveolar macrophages in the lung as a result of smoke inhalation. In RB, pigmented macrophages accumulate focally surrounding small airways [ 50 ], whereas in DIP, pigmented macrophages accumulate more diffusely throughout the lung parenchyma [ 51 ].

RB usually consists of ill-defined ground-glass nodules of varying size 1—10 mm generally in an upper lung zone distribution, whereas DIP is generally characterized by more extensive GGOs, tends to be more pronounced in the lower lobes, and may have a fibrotic component manifested by traction bronchiectasis and volume loss Figure 3 A [ 45 , 51 ]. However, based on our current understanding of RB and DIP, this term is thus a misnomer since these abnormal cells are in reality pigmented alveolar macrophages.

PLCH is recognized by distinctive radiographic and histopathologic findings in a patient with a history of smoking. Histopathologic findings of PLCH include stellate shaped nodules with chronic inflammatory cell accumulation, the hallmark of which is the accumulation of CD1a-positive histiocytes referred to as Langerhans cells [ 53 ]. Radiographically, the findings of PLCH occur in an upper lobe-predominant distribution and are often striking, consisting of a combination of various sized lung nodules and bizarre-shaped cysts, both of which give PLCH its distinct appearance [ 45 ].

SRIF refers to emphysematous air spaces with abnormally thick fibrotic walls. Typically, straight-forward upper lobe-predominant centrilobular emphysema secondary to smoking presents radiographically as enlarged air spaces with no true discernable walls. In SRIF, the walls of these emphysematous spaces are abnormally thick, well-defined, and contain excess collagen, thus being most consistent with smoking-induced fibrosis which surrounds emphysematous spaces [ 54 , 55 ].

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This process has also been referred to as airspace enlargement with fibrosis, which seems descriptively more accurate [ 2 ], but smoking-related interstitial fibrosis SRIF seems to have gained more acceptance [ 56 ]. Over the last decade, one other entity related to smoking-induced lung injury which has gained attention has been termed combined pulmonary fibrosis and emphysema CPFE [ 57 ]. Though somewhat non-specific in terms of distribution of disease, this term has generally been used to describe centrilobular emphysema in the upper lobes and lung fibrosis in the lower lobes [ 58 ].

Of note, in SRIF described above, the fibrosis component is observed in a similar distribution as the emphysema [ 54 , 55 ], and it thus seems straight forward to conclude that tobacco smoke is a direct cause of the fibrotic change [ 59 ]. With upper lobe emphysema and lower lobe fibrosis, such as in CPFE, it is difficult to attribute the fibrotic change with certainty to tobacco smoke. The first-line therapeutic approach for all forms of lung injury due to tobacco smoking or other inhalants is smoking cessation [ 56 ].

In patients with progressive disease, consideration of anti-inflammatory therapy with systemic corticosteroids is appropriate, though efficacy of such treatment for any of the smoking-related ILD forms has not been convincingly demonstrated [ 49 , 61 ]. HP, also referred to as extrinsic allergic alveolitis, is one of the most important ILDs to recognize due to possible environmental interventions or remediations which could provide substantial patient benefit [ 62 ].


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HP results from an exuberant immunologic response to inhalation of environmental organic antigens [ 63 ], originating most commonly from exposure to avian proteins [ 64 ], mold [ 65 ], or farming [ 66 , 67 ]. Some forms of HP may result from inhalation of inorganic antigens [ 68 , 69 ], but most implicated antigens are organic in nature.

The recognition and identification of the etiology of HP rests almost solely on a detailed environmental, avocational, and occupational history [ 70 ]. Specific attention needs to be directed at the possibility of mold infestation in the home or work environment [ 71 ]. Clues in this regard include a history of water intrusion into the premises, damp or musty spaces, musty odor, or visible mold infestation. In some instances, inspection of the premises by a certified industrial hygienist will allow accurate assessment as to the presence of mold infestation and provide guidance for potential remediation if necessary [ 72 ].

Additionally, patient-directed questions regarding exposure to avian proteins are essential, and should assess not only birds residing within the household, but potentially frequent contact with birds or bird excrement outside of the home such as in coops, chicken houses, and other similar dwellings [ 73 , 74 ]. Different panels of serum precipitating antibodies directed at common environmental and avian antigens are commercially available, and although their utility remains a source of debate due to low sensitivity and specificity, a positive test in the appropriate clinical setting helps support the diagnosis of HP [ 63 ].

It is important to note that in some instances, despite a comprehensive environmental, avocational, and occupational history by experienced physicians, identification of a precise antigen in patients with clinical presentation highly suggestive of HP may be difficult [ 75 , 76 ]. HP can present in an acute, subacute, or chronic manner, but often manifests as insidious ILD of uncertain etiology. In this instance, radiographic findings are often present in an upper lobe-predominant fashion, and often accompanied by typical findings of fibrosis [ 38 , 77 ]. A mosaic attenuation CT pattern is also supportive of chronic HP Figure 3 B , in which areas hyperattenuated lung are interspersed with areas of hypoattenuated lung, and likely represents sequela of small airways injury and focal air trapping.

colby the coal mining bee Manual

The hypoattenuated areas are often accentuated when expiratory imaging protocols are additionally applied [ 77 ]. Histopathologic findings in HP consist of chronic inflammation centered around small airways, and the presence of poorly-formed granulomas Figure 2 , panels G,H. Poorly-formed granulomas noted on a lung biopsy specimen should always prompt consideration of HP as a diagnosis.

Therapeutic interventions for chronic HP involve most importantly cessation of the inciting exposure [ 78 ]. In the case of avian-related HP, complete cessation of all exposure to avian proteins is crucial [ 79 ], and a thorough professional cleaning of the environment needs to be undertaken if the patient is to remain within that environment [ 80 ].

It should be noted that even following professional cleaning, significant avian products may remain detectable in the environment [ 64 ]. In the case of mold, remediation of the environment in attempt to cease water intrusion and remove mold infested materials is of utmost importance [ 72 ]. This work should be performed by a professional company with remediation expertise since significant antigen dispersion into the environment may occur during this process. The role of corticosteroids and other immunosuppressive agents in chronic HP is not completely defined.

Numerous reports do suggest improvement in clinical status and PFTs with corticosteroids [ 81 , 82 ], though other reports have indicated minimal to no improvement [ 83 ]. Likewise, the role of alternative immunosuppressive therapies such as mycophenolate mofetil or azathioprine remains to be proven at the present time [ 81 , 84 ]. Some reports suggest that response to anti-inflammatory therapy in particular patients may be predicted based on radiographic features which are present or absent on chest CT imaging at presentation [ 85 ].

Although there may be strict differences between CTD and autoimmune disease, we will use these terms interchangeably in this review. It is particularly important to identify CTD disease as the inciting ILD etiology due to the high likelihood of physiologic improvement with corticosteroids and other immunosuppressive agents [ 32 , 86 ].

1. Introduction

The American Thoracic Society and European Respiratory Society have addressed this entity by designating it interstitial pneumonia with autoimmune features [ 91 ]. The pathophysiology of CTD—ILD likely involves repetitive and progressive lung injury due to systemic inflammation [ 92 ], and the pathophysiologic role of a secondary insult from inhalation of various substances remains to be discerned [ 93 , 94 ].

The recognition and identification of patients with CTD-ILD occurs mostly from a constellation of the medical history, physical exam, radiologic, and serologic findings. A history of constitutional symptoms, arthralgias, arthritis, rashes, and other systemic symptoms may suggest the possibility of an underlying CTD, and physical exam findings specific to a particular CTD are often very helpful [ 86 , 95 , 96 , 97 ].

In the appropriate clinical context, serologic markers of autoimmunity are very helpful in understanding the likely pathobiology of the ILD. It has been somewhat controversial in the past as to whether all patients with ILD should undergo a full CTD serologic evaluation looking for evidence of autoimmune disease [ 91 , 98 ]; most consensus statements do support this approach, and it is our belief as well that almost all patients with ILD should undergo such testing as it can have profound impact on therapeutic management and prognosis [ 2 , 4 , 6 , 91 ]. Table 2 shows a list of suggested autoimmune serology and additional assays that can be considered in the work-up of patients with ILD.

The opacities often have a pattern in which the extreme periphery of the lung is spared Figure 3 D [ 99 ]. Most patients with CTD-ILD will not require a lung biopsy, since treatment response and prognosis are likely to be determined more by the presence of ILD secondary to CTD rather than the specific histopathologic pattern that happens to be present [ 32 , , , , ]. In selected instances, bronchoscopy with BAL may be useful to exclude infection and to evaluate the degree of active alveolitis [ , ].

Arguably, patients with ILD secondary to CTD have the best responses to immunosuppressive therapy compared to other ILD groups [ 32 , 87 , , , , , , ]. Corticosteroids have long been the mainstay of immunosuppressive therapy for patients with CTD-ILD [ , ], however clinical experience and research studies have shown additional benefits of steroid-sparing agents, such as azathioprine [ , , ], methotrexate [ , ], cyclophosphamide [ , , , ], and more recently, mycophenolate mofetil [ , , , , ].

Over the past five years, mycophenolate mofetil has gained widespread acceptance for use in patients with CTD-ILD as it is generally well-tolerated and efficacious [ , , , , , ]. This syndrome presents as one of the inflammatory myopathies—PM or DM—in combination with the presence of one or more anti-aminoacyl-tRNA synthetase antibodies on serologic testing, and the presence of radiographic ILD [ ].