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A major factor that explains the importance of emotional branding is related to consumer experience. No longer are consumers focusing on product specifics or service satisfaction; they seek experiences from a brand they like. In experiencing a brand, whether it is a product, service, or a retail store, consumers do not just look for quality or low prices; they want to gain emotional rewards from enticing store atmosphere, superb customer service, and entertaining experiences. They also want to express who they are and the relationships that are important to them through consuming or supporting a specific brand (Kim et al. 2014; Kumar and Kim 2014).

Fluid resuscitation strategies for combat casualties need to be urgently refined to keep pace with current recommendation. Large volume crystalloid resuscitation which is still in vogue in the most situations in combat need to be replaced with low volume colloid resuscitation and one of plasma or FWWB as forward in the field as possible to satisfy the arms of DCR namely the hypotensive resuscitation and haemostatic concerns. There should be a policy to outline planning parameters for blood supply to Forward medical echelons. The policy should specify zone wise responsibilities at various levels for ensuring availability of blood and blood products including collection, storage and transportation to meet operational requirements.

The term corneal dystrophy embraces a heterogenous group of bilateral genetically determined non-inflammatory corneal diseases that are restricted to the cornea. The designation is imprecise but remains in vogue because of its clinical value. Clinically, the corneal dystrophies can be divided into three groups based on the sole or predominant anatomical location of the abnormalities. Some affect primarily the corneal epithelium and its basement membrane or Bowman layer and the superficial corneal stroma (anterior corneal dystrophies), the corneal stroma (stromal corneal dystrophies), or Descemet membrane and the corneal endothelium (posterior corneal dystrophies). Most corneal dystrophies have no systemic manifestations and present with variable shaped corneal opacities in a clear or cloudy cornea and they affect visual acuity to different degrees. Corneal dystrophies may have a simple autosomal dominant, autosomal recessive or X-linked recessive Mendelian mode of inheritance. Different corneal dystrophies are caused by mutations in the CHST6, KRT3, KRT12, PIP5K3, SLC4A11, TACSTD2, TGFBI, and UBIAD1 genes. Knowledge about the responsible genetic mutations responsible for these disorders has led to a better understanding of their basic defect and to molecular tests for their precise diagnosis. Genes for other corneal dystrophies have been mapped to specific chromosomal loci, but have not yet been identified. As clinical manifestations widely vary with the different entities, corneal dystrophies should be suspected when corneal transparency is lost or corneal opacities occur spontaneously, particularly in both corneas, and especially in the presence of a positive family history or in the offspring of consanguineous parents. Main differential diagnoses include various causes of monoclonal gammopathy, lecithin-cholesterol-acyltransferase deficiency, Fabry disease, cystinosis, tyrosine transaminase deficiency, systemic lysosomal storage diseases (mucopolysaccharidoses, lipidoses, mucolipidoses), and several skin diseases (X-linked ichthyosis, keratosis follicularis spinolosa decalvans). The management of the corneal dystrophies varies with the specific disease. Some are treated medically or with methods that excise or ablate the abnormal corneal tissue, such as deep lamellar endothelial keratoplasty (DLEK) and phototherapeutic keratectomy (PTK). Other less debilitating or asymptomatic dystrophies do not warrant treatment. The prognosis varies from minimal effect on the vision to corneal blindness, with marked phenotypic variability.

The term corneal dystrophy refers to a heterogenous group of genetically determined corneal diseases that are restricted to the cornea (Table 1). The designation corneal dystrophy is imprecise but remains in vogue because of its clinical value. Typically, the conditions included under the umbrella of corneal dystrophy are bilateral spontaneous corneal disorders that vary in clinical severity and in their signs and symptoms. Most corneal dystrophies have no systemic manifestations and present with variable shaped corneal opacities in a clear or cloudy cornea and they affect visual acuity to different degrees. Diagnoses can be established on clinical grounds and this may be enhanced with studies on surgically excised corneal tissue and in some cases with molecular genetic analyses. The management options and outcomes following therapy vary with the condition under consideration. Clinically, the corneal dystrophies are classified with respect to the layer of cornea involved and can be divided into three groups based on the sole or predominant anatomical location of the abnormalities. Some affect primarily the corneal epithelium and its basement membrane or Bowman layer and the superficial corneal stroma (anterior or superficial corneal dystrophies), the corneal stroma (stromal corneal dystrophies), or Descemet membrane and the corneal endothelium (posterior corneal dystrophies). Most of the corneal dystrophies are of Mendelian inheritance (autosomal dominant, autosomal recessive or X-linked recessive) with some phenotype diversity and a variable degree of penetrance. The age of onset of the different types of corneal dystrophies is variable and reflects different underlying pathogenic defects (Table 2). A few corneal dystrophies are congenital and represent developmental anomalies.

Reis-Bucklers corneal dystrophy. Light microscopic view of abnormal deposit of fuschinophic mutated transforming growth factor beta induced protein in the superficial corneal strome. Masson trichrome stain (Courtesy of Dr. Guy S. Allaire).

Reis-Bücklers corneal dystrophy. Light microscopy of cornea showing characteristic red stained deposits of mutated transforming growth factor beta induced protein in the superficial corneal stroma. In this specimen they extend deeper into the corneal stroma than the abnormal deposits of Figure 6. Masson trichrome stain.

The corneal opacities in GCD are readily visualized in the excised cornea (Figure 32). The light microscopic and TEM appearance and staining attributes of the corneal deposits in GCD are diagnostic. Eosinophilic lesions deposit in the cornea in GCD (Figure 33). The corneal opacities consist predominantly of an extracellular deposition of mutant transforming growth factor beta induced protein (TGFBIp), which stains a brilliant red with the Masson trichrome stain [63] (Figures 34 and 35). With the Wilder reticulin stain, the accumulations contain tangles of argyrophilic fibers. The deposits react with histochemical methods for protein as well as with antibodies to TGFBIp (Figure 36). The granules stain positively with luxol fast blue and are reported to stain positively with antibodies to microfibrillar protein.

PPCD is an autosomal dominant genetically heterogenous entity with extremely variable expression. Three genes have been implicated in PPCD (VSX1, COL8A2, TCF8), but the evidence implicating VSX1 and COL8A2 is questionable. p. Leu159Met and p. Gly160Asp mutations in VSX1 have also been reported [134], but an analysis of two large families in the Czech republic has shown that the locus excludes the VSXI gene [135]. A missense p. Gln455Lys mutation in the COL8A2 has also been identified in PPCD, but a tissue diagnosis in that family was not documented [120]. Evidence for TCF8, which encodes transcription factor 8, is much more convincing [136].

Resilience is ubiquitous in everyday speech, academic literature and governmental policies. Yet it seems to have taken a narrow scope in healthcare, confined to individual and psychological resilience. This short essay aims to broaden the understanding of resilience to organisational levels and calls intensivists to take active roles in fostering resilience for their staff. The article explores firstly the background and etymology of resilience. It then challenges current approaches and briefly signposts some current work in the area. Some examples of structural factors which build individual resilience are listed, followed by a call for intensivists to take active roles to build future resilience. The need for interdisciplinary, cross-sectoral and multi-level approaches is vital to build future healthcare resilience, and we intensivists must continue to be advocates for systemic change.

We should know better than to apply one-dimensional solutions to multi-faceted problems. Resilience cannot merely be confined to individual interventions. Fortunately, there is slow but increasing recognition of the interdisciplinary, cross-sectoral and multi-level (nicely abbreviated as ICM) approaches required to build true resilience. On an organisational level, resilience has been intricately tied to patient safety paradigms, and its definition spans across a crisis, encompassing the ability to anticipate, respond, monitor and learn from shocks [3]. In that sense, perhaps we should be taking a more organisational perspective of resilience-building, reframing the patient-safety lens to include staff-safety too, and not limiting provisions to the confines of a crisis. The Intensive Care Society is undertaking research to better understand such systemic factors affecting individual well-being and resilience [4]. Universities are also taking notice, with studies on practical factors that build staff resilience. Even the NHS operational strategy for 2022/23 specifically considers how we can adapt to the flexible working needs of the modern healthcare professional [5]. 2b1af7f3a8

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