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Chronic laminitis in the Kaimanawa feral horses of New Zealand. BA Hampson 1*, MA de Laat 1, Beausac C 2 ,Rovel T 2 and CC Pollitt 1 1 The Australian Brumby Research Unit, School of Veterinary Science, The University of Queensland, Gatton Campus, Qld 4343, Australia. 2 National Veterinary School of Toulouse, France. *Corresponding author: b.hampson1@uq.edu.au Key words: equine, laminitis, histomorphology, histopathology, feral Introduction Equine laminitis is responsible for dysfunction and disruption in the working life of many horses. In its most severe form the disease can culminate in euthanasia of an affected horse. Laminitis occurs in both acute and chronic forms and the lesions of both forms have been described previously (Pollitt 1996, Eckfalk 1992, Van Eps 2009, Obel 1948). In the acute phase, the disease is characterised by lengthening, thinning and tapering of the tips of the lamellae, and separation of the lamellae from the basement membrane (Pollitt, 1996, Johnston et al 1998). Following an acute episode of laminitis the various tissues of the suspensory apparatus of the distal phalanx mount a healing response the outcome of which depends on the severity of the initial insult and the magnitude of the mechanical load exerted on the foot (Van Eps and Pollitt, 2009). Van Eps and Pollitt (2009) described the histopathology of laminitis in the post acute phase seven days after dosing to induce laminitis. Although there was marked disruption in lamellar architecture, the lamellar tissue had reorganised rapidly following the initial disruption, compared to observations made 48 h after dosing (Pollitt, 1996, Pollitt and Daradka, 2004). The chronic form of the disease is characterised histologically by dysplastic degeneration of the secondary epidermal lamellae (SELs), the formation of cap horn over the primary dermal lamellar (PDL) tips, and proliferation of immature tubular horn contributing to lamellar wedge formation (Roberts et al, 1980, Morgan et al,1999, Collins et al, 2010). The lamellar wedge contributes to misalignment of the hoof wall and distal phalanx, and often accompanies chronic laminitis (Roberts et al 1980, Van Eps and Pollitt, 2009, Collins et al, 2010). The incidence of laminitis has been described in several domestically managed horse populations (Treiber et al 2006). However, few studies have reported the incidence of the chronic form of the disease. Animal husbandry practices such as over-feeding and confinement have been blamed for the increasing incidence of laminitis in managed horses (Pollitt 2008). However, Hampson et al (2010) also observed clinical evidence of chronic laminitis in feral horses from the Kaimanawa area of New Zealand, but this was not confirmed histologically. Confirmation and histopathological description of the disease in this population is important, as these horses are free roaming and exempt from human intervention. The Kaimanawa horses have been isolated for several decades and are considered a closed population (Taylor, 1990). They roam a vast area and have free access to both native and introduced pasture species (Linklater, 2000). Confirmation of chronic laminitis, by histopathologic assessment, in this free roaming population would confirm the vulnerability of Equids to the disease even when feral. The current study facilitates a better understanding of the risks of pasture-associated laminitis in all horses. Materials and methods Animals Fifty-six feral horses from the Kaimanawa Ranges of New Zealand (28 stallions and 28 mares) aged over six years were randomly selected for use in this study following mustering and euthanasia,. Horses were culled for reasons other than research. Kaimanawa horses are small (adult wither height is 133-151 cm) (Linklater, 2000) and are descendants of Welsh and Exmoor ponies that have inter-bred with local farm and cavalry horses (Taylor, 1990). Genetic analysis suggests that they are now closely related to domestic Thoroughbred and local station hacks (Halkett, 1991). The Kaimanawa horses occupy 700 km2 of upland plateaux, steep hill country, river basins and valleys (Rogers, 1991). Minimum temperatures range from -100 to 70C, and the maximum ranges from 120 to 320C throughout the year. Rainfall ranges from 75 to 180 mm/month and averages 100 mm/month. Kaimanawa horses prefer to graze red tussock grasslands in the autumn and winter seasons, whereas exotic sheep pasture grasses are eaten in the winter and spring (Linklater, 2000). Histology The left forefoot of each horse was removed and processed for histology within 60 minutes of death. A 30mm, full thickness mid-sagittal sample of the dorsal hoof wall including lamellae was taken 3mm proximal to the distal tip of the distal phalanx. Samples were immediately placed in 10% neutral buffered formalin. Prior to further processing by routine methods, a tissue block measuring 5mm wide was cut from the centre of the 30mm sample. Following embedding in paraffin wax, a mid-sample lamellar tissue block which originated approximately 18mm proximal to the tip of the distal phalanx was sectioned transversely at 5µm, mounted on Superfrost Plus slides (Menzel)1 and stained with haematoxylin and eosin. Sections were examined using light microscopy (Olympus BX-50)2. Histopathology One author (CCP), who is experienced in describing lamellar histopathology, assessed the presence of laminitis, ranked the laminitis grade (nil, acute, mild chronic, moderate chronic, severe chronic) and then described the histopathological lesions. Histomorphology Following histopathology assessment and grouping of horses into laminitic and nonlaminitic groups, 15 horses from each group were randomly selected for histomorphological analysis. Randomisation and coding of all sections was performed prior to measurement. Two authors (TR and CB), blinded to each other and to the sample origin, individually performed measurements of PEL and SEL according to the following protocol. Four sets of measurements were made using image analysis computer software; total primary epidermal lamellar length (TPELL), keratinised primary epidermal lamellar length (KPELL), the length of the SEL at the base (proximal, SELLB) and tip (distal, SELLT) of each PEL. Eight PEL were measured on each section at 20 X magnification to determine TKELL and TPELL (Fig 1a). Ten randomly selected SEL were measured at 100 X magnification both proximally (10 – 30%) and distally (70 – 90%) on each selected PEL (Fig 1b). Histological evidence of PEL architectural variation The same sections (n = 30) were then subject to further analysis. Three authors (BH, TR, CB) used light microscopy to collectively assess each sample to determine the number of immature (shorter than average PEL with a pointed PEL tip), mature PELs and the number of branched keratinised PEL in both the axial and abaxial half of each PEL. Ethical approval and statistical analyses The project was approved by the University of Queensland Animal Ethics Committee (AEC-PCA) (approval number SVS/393/07/AHF) which ensures compliance with the Animal Welfare Act of Queensland (2001) and the Australian Code of Practice for the Care and Use of Animals for Scientific Purposes (7th edition 2004). Epidermal lamellar measurements were analysed for observer one (CB). Epidermal measurements were compared between groups using a Welch t-test. Within groups, average SELL was compared between proximal and distal locations using a Welch ttest. The level of agreement between the two observers was assessed with Bland- Altman’s Limits of Agreement (LOA) and Lin’s concordance co-efficient (?c). Pearson’s correlation coefficient was used to assess the random variation of interrater agreement. All data are presented as mean ± se. Statistical significance was set at p < 0.05. Statistical analyses were performed using R version 7.2.7. Results Histopathology Within the Kaimanawa feral horse population sampled (n = 56) 45% (n = 25) were diagnosed with chronic laminitis. Of the horses with laminitis, 60% (n = 15) were assessed as mild chronic, 32% (n = 8) as moderate chronic, 8% (n = 2) as severe chronic and 8% (n = 2) were judged to have acute lesions superimposed on preexisting chronic laminitis. Of the horses diagnosed with chronic laminitis, the most prevalent histopathologic features were attenuated SELs, multi-branched SELs, dystrophic PEL tips (axial end) and the presence of cap horn (Table1, Figure 1). A combination of these and other features was used to subjectively grade the severity of laminitis. Table1. The incidence of the histopathologic features of laminitis in horses diagnosed with chronic laminitis (n = 25) in a sample population of feral horses (n = 56, 28 male, 28 female, aged > 6 years) from the Kaimanawa Ranges in New Zealand. Histopathology feature Number of samples % of samples (n = 25) Attenuated SELs 11 44 Presence of Island SELs 5 20 Attenuated PEL tips (axial) 5 20 Multi-branched SELs 13 52 Dystrophic PEL tips (axial) 8 32 Basement membrane separation 2 8 PDL oedema 2 8 Lamellar wedge/cap horn 16 64 Histomorphology The inter-rater agreement between the observers was considered acceptable (Table 2). Histomorphological assessment of the lamellar architecture revealed a trend towards increased length of the keratinised axis and total length of the PEL in chronic laminitic horses when compared to non-laminitic horses. However, there was no statistical difference in morphological measurements between the normal and laminitic groups for any parameter (Table 2). No difference in the degree of proliferative PEL changes was seen between the non-laminitic and laminitic groups (Table 3). Table 2: Mean ± se epidermal lamellar length (µm) measured by observer 1 (CB) in feral horses (n = 30) from the Kaimanawa Ranges area of New Zealand. One group of horses (n = 15) showed histopathological evidence of laminitis (Pathology) while the other group (n = 15) appeared to have normal lamellae (Normal). Measurements were made on the left forefoot of each horse. Total and keratinised primary epidermal lamellar length (PELL) and secondary epidermal lamellar length (SELL) was measured at the base and tip of the PEL. The inter-rater agreement between two observers who each measured all of the parameters was determined with Lin’s concordance co-efficient (?c) and Bland-Altman’s Limits of Agreement (LOA). Pearson’s correlation coefficient (r) was used to assess the random variation of inter-rater agreement. Parameter KPELL TPELL SELLB SELLT Pathology 2877 ± 102 3375 ± 120 229 ± 16.5 195 ±12.4 Normal 2698 ± 68.7 3096 ± 86.5 226 ± 10.6 169 ± 11.1 Lin’s ?c 0.86 0.83 0.80 0.78 LOA (µm) 61.5 82.9 10.2 19.5 % in 95% CI 92.3 96.2 93.4 91 Pearson’s r 0.90 0.85 0.83 0.83 Key: TPELL: total primary epidermal lamellar length, KPELL: keratinised primary epidermal lamellar length, SELLB: length of the secondary epidermal lamellae at the abaxial end of the PEL, SELLT: length of the secondary epidermal lamellae at the axial end of the PEL Table 3. The presence of PEL branching in Kaimanawa horses with (n =15) and without (n =15) histopathological signs of laminitis. Quantification of lamellar branching is expressed as the number of branches per 100 lamellae examined. No difference in the degree of PEL branching was seen between the non-laminitic and laminitic groups Immature PELs Keratinised PEL branching in the proximal 50% of PEL Keratinised PEL branching in the distal 50% of PEL Non-laminitic Group (N=15) 13.9 7.3 2.2 Laminitic Group (N=15) 13.5 4.8 2.8 Discussion The equine foot has evolved into a complex organ requiring that all of its components work together as an integrated unit (Grosenbaugh, et al, 1999). The suspensory apparatus of the distal phalanx unites the distal phalanx to the lamellar epidermis and constitutes the principal mechanism by which biomechanical forces in the distal limb are accommodated and resisted (Collins et al, 2010). However, the critical load bearing function of this organ places the foot at risk of injury and disease, particularly when affected by an insult that compromises lamellar integrity, such as laminitis. The epidermal lamellar layer responds rapidly to an acute insult with hyperplasia (Roberts et al 1980) and reorganisation of lamellar epidermal basal cells and their basement membrane (van Eps and Pollitt 2009). Despite this healing response, disruption and dysfunction of the suspensory apparatus may result, especially when an acute laminitis episode has been severe. Regardless of the type of lamellar change present, the ultimate strength and elasticity of the suspensory apparatus is reduced to some extent (Hood, 1999, Morgan, 1999). Hood (1999) reported that the strength of the lamellar interface in manageable cases of chronic laminitis may be as low as 60%. These changes have a severe impact on the function of the digit and the ability of the horse to maintain sound locomotion. The current study found a high incidence of histopathological changes indicative of laminitis in the left fore-feet of feral Kaimanawa horses. The histological presentation was similar to that reported previously in domestic horses suffering chronic laminitis (Roberts et al, 1980, Morgan et al, 1999, van Eps 2009, Collins et al, 2010). The most likely reason for the high incidence of laminitis in the Kaimanawa population is selective grazing for highly palatable exotic sheep pasture grasses high in nonstructural carbohydrates (Watts and Pollitt 2010, Hampson, 2010). Long day lengths at high altitude in the Kaimanawa Ranges coupled with temperatures below freezing produce the ideal scenario for pasture-induced laminitis (Pollitt and Watts 2010, Hampson, et al, 2010,). Another potential explanation for the high incidence of chronic laminitis in this population is the possibility that the Kaimanawa feral horses are insulin resistant. Hyperinsulinaemia in horses is capable of causing lamellar architectural changes similar to those reported in the current study (de Laat et al, 2010). It is known that pony breeds are at a higher risk of developing insulin resistance (Jeffcott, 1986) and the Kaimanawa feral horses are direct descendents of Welsh and Exmoor ponies. However, the Kaimanawa feral horses were gracile and athletic and did not exhibit an overtly insulin resistant phenotype; the incidence of insulin resistance in this population is unknown. Further, the presence of a high incidence of insulin resistance in horses in a feral horse population with a long history of access to plentiful, energy-rich pasture is counterproductive. Further work to determine the presence of insulin resistance in feral horse populations is required. It is an important finding that the feral horse lifestyle in the environment of the Kaimanawa Ranges in New Zealand is no protection against foot disease. The finding suggests that horses are vulnerable to laminitis whether in domestic care or in a feral habitat. Roberts et al (1980) characterised histopathologic changes in chronic laminitis (n = 8) as overall PEL architectural deformation, SEL hyperplasia with pearl-like epithelial formation in the dermis, and PEL hyperkeratinisation, producing a wedge of epidermis between the distal phalanx and the hoof wall. The observations of the current study were very similar and included the presence of lamellar wedge/cap horn production, multi-branching of SELs at the axial tips of the PELs, attenuated SELs, the presence of dystrophic PEL axial tips, the presence of attenuated and pointed PEL axial tips and the presence of islands of SELs disconnected from the PEL. Morgan, et al (1999) found that lamellar architectural changes were restricted to the SELs in cases of mild pathology but involved the PELs when the severity of the insult increased. Hyperplasia of the PELs was more pronounced abaxially, whereas SEL hyperplasia was more common axially, nearest to the distal phalanx. Histologicallly, lengthening of the lamellar interface correlates with a radiographical increase in the distance between the dorsal surfaces of the DP and the outer hoof wall and a detectable lamellar wedge (Morgan, et al, 1999). Our study found only a trend towards increased keratinised (KPELL) and total primary epidermal lamellar length (TPELL) in the horses with histological changes consistent with chronic laminitis. SEL lengths at the base (abaxial) and tip (axial) of the PEL were similarly elongated. A previous report of histomorphology of the PEL at seven days following induction of laminitis reported that the keratinised axis of the PEL was not affected (van Eps and Pollitt, 2009). Other studies of laminitis in the acute phase of the disease have shown similar results (Linford 1987 , Sarrat and Hood, 2005 ). In a study of traumatically induced laminitis over a four month period, Linford (1987) reported keratinised PEL axis and total PEL lengthening as well as SEL attenuation at the PEL axial tips which may indicate that PEL changes are more likely to occur in chronic disease. However, data on lamellar morphology in chronic laminitis is scarce. The lack of significant SEL length difference between laminitic and non-laminitic horses in our study was unexpected. Based on previous studies {Asplin, 2010}, we expected secondary epidermal lamellar length to be increased in the laminitic group, particularly at the PEL axial tips. However, there is currently no reported SEL length data in chronically laminitic horses available for comparison. It is possible that in horses with chronic laminitis, the SELs adjust to the laminitic insult and reverse the attenuation seen in acute phases. However, we recognised lamellar separation in a number of the laminitic samples from the Kaimanawa population. Lamellar separation was characterised by remnants of empty basement membrane at PEL axial tips, indicating that the PEL axial tip was originally situated more abaxially than the current position (Figure 1). Measurements of the “original length” of the PEL indicated a 5-30% shortening of the PEL after lamellar separation. Separated PEL were also characterised by a wavy appearance of the PEL axis, further suggesting PEL shortening following lamellar separation. Lamellar separation and PEL shortening in some of the samples, may explain why significant morphometric differences were not obtained in this study. In tissue affected by lamellar separation, displaced SELs are no longer under tension and may have responded by shortening to near-normal length. Another possibility is that horses classified as non-laminitic during histopathological examination were actually suffering mild laminitis but lesions were considered insufficient for diagnosis. As a result, SELs in all horses sampled may have been attenuated to some degree and masked a measureable difference. It may be that if the environment of the Kaimanawa Ranges caused detectable chronic laminitis in 46% of the population, then the entire population was, or has been, affected to some degree. Epidermal architectural changes were absent in normal control horses in previous studies (Roberts et al, 1980), van Eps (2009). Sarratt and Hood (2005) reported SEL bifurcation in normal feet occurred more frequently in the proximal region, near the coronet, and was much reduced distally where our samples were located. Linford (1987) noted only the “occasional” presence of short, immature PELs with lengths of one-half to two-thirds of the majority of the lamellae. He also noted “occasional” forked or bifurcated PEL proximally that continued distally. The presence of immature PELs and axial and abaxial keratinised axis branching of PELs was common in both of our laminitic and non-laminitic horses. It is difficult to compare our quantitative data on lamellar architecture with previous studies reporting subjective assessments but our observation was that the changes seen in the Kaimanawa population were beyond “occasional”. The changes may suggest abnormal lamellar proliferation at the coronary band in response to a stressor, such as a laminitic insult, which further supports the possibility that all horses in the population were affected to some degree. Using histopathology the current study introduces a novel approach of quantifying lamellar changes associated with chronic laminitis. Further data may become available in the future to allow these architectural changes to be more completely understood. The current study appears to be the first to confirm histologically that chronic laminitis occurs in feral horses. This is an important observation as it supports the hypothesis that E. caballus is vulnerable to the insult of laminitis, irrespective of its state of domestication. The physiological and bio-engineering adaptations of the equine foot, that allow horses such high speed and agility, may have come at the price of vulnerability. The aetiology of the chronic laminitis described in this study is potentially linked to pasture-based nutrition. As Kaimanawa feral horses have unlimited access to pasture and browse through all seasons of the year, the importance of controlled nutrition for laminitis prevention is highlighted. Footnotes 1 Menzel, Braunschweig, Germany. 2 Olympus Corporation Lifesciences, Japan. 3 Image J References Asplin, K.E., Patterson-Kane, J.C., Sillence, M.N., Pollitt, C.C., Mc Gowan, C.M., 2010. Histopathology of insulin-induced laminitis in ponies. Equine Veterinary Journal, no-no. Collins, S.N., van Eps, A.W., Pollitt, C.C., and Kuwano, A. (2010) The lamellar wedge. Vet Clin North Am Equine Pract. Advances in Laminitis, Part 1. 26(1), 179-195. Daradka, M., and Pollitt, C.C. (2004) Epidermal cell proliferation in the equine hoof wall. Equine Vet J 36, 236-241. de Laat, M.A., McGowan, C.M., Sillence, M.N. and Pollitt, C.C. (2010) Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses. Equine Veterinary Journal 42, 129-135. Ekfalck, A., Rodriguez, H. and Obel, N. (1992) Histopathology in post-surgical laminitis with a peracute course in a horse. Equine Veterinary Journal 24, 321-324. Grosenbaugh, D.A., Morgan, S.J. and Hood, D.M. (1999) The digital pathologies of chronic laminitis. Vet Clin North Am Equine Pract. 15, 419-436. Halkett, J.R. (1996) A genetic analysis of the Kaimanawa horses and comparisons with other equine types. Master of Science in Genetics, Massey University, New Zealand. Hampson, B.A., Ramsey, G., Macintosh, A., Mills, P., de Laat,M.A., Pollitt, C.C (2010) Morphometric variables and incidence of abnormalities in the feet of Kaimanawa feral horses. AVJ 88, 124-131. Hood, D.M. (1999) The mechanisms and consequences of structural failure of the foot. Veterinary Clinics of North America-Equine Practice 15, 437. Jeffcott, L.B., Field, J.R., McLean, J.G., Odea, K., 1986. Glucose Tolerance and Insulin Sensitivity in Ponies and Standardbred horses. Equine Veterinary Journal 18, 97-101. Johnson, P.J., Tyagi, S.C., Katwa, L.C., Ganjam, V.K., Moore, L.A., Kreeger, J.M. and Messer, N.T. (1998) Activation of extracellular matrix metalloproteinases in equine laminitis. Vet Rec 142, 392-396. Linford, R.L. (1987) A Radiographic, Morphometric, Histolocal and Ultrastructural Investigation of the Lamellar Function, Abnormality and the Associated Radiographic Findings For Sound and Footsore Thoroughbreds, and Horses With Experimentally Induced Traumatic and Alimentary Laminitis. PhD Thesis. University of California, Davis, USA. Linklater, W.L., Cameron, E.Z., Stafford, K.J. and Veltman, C.J. (2000) Social and spatial structure and range use by Kaimanawa wild horses (Equus caballus: Equidae). New Zealand Journal of Ecology 24, 139-152. Morgan, S.J., Grosenbaugh, D.A. and Hood, D.M. (1999) The pathophysiology of chronic laminitis. Pain and anatomic pathology. Vet Clin North Am Equine Pract 15, 395-417, vii. Obel, N. (1948) Studies of the Histopathology of Acute Laminitis., Almgvist and Wilcsells Bottrykeri Ab Uppsala (Thesis). Pollitt, C.C. (1996) Basement membrane pathology: a feature of acute equine laminitis. Equine Veterinary Journal 28, 38-46. Pollitt, C. (2008) Equine Laminitis. Current Concepts., RIRDC publication, Canberra. p 100. Pollitt, C.C. and Watts, K. (2010) Equine Laminitis. Managing pasture to reduce risk of laminitis. RIRDC publication, Union Offset Printing , Canberra, 38-40. Roberts, E.D., Ochoa, R. and Haynes, P.F. (1980) Correlation of dermal-epidermal lamellar lesions of equine hoof with various disease conditions Vet. Pathol. 17, 656-666. Sarrat, S.M. and Hood, D.M. (2005) Evaluation of architectural changes along the proximal top distal regions of the dorsal laminar interface in the equine hoof. Am J Vet Res 66, 277-283. Taylor, R.H. (1990) Feral horse. In: The handbook of New Zealand mammals, Oxford University Press, Auckland, New Zealand. pp 99-113. Treiber, K.H., Kronfeld, D.S. and Geor, R.J. (2006) Insulin Resistance in Equids: a Possible Role in Laminitis. The Journal of Nutrition Supp, 2094S-2098S. van Eps, A.W. and Pollitt, C.C. (2009) Equine laminitis model: Lamellar histopathology seven days after induction with oligofructose. Equine Veterinary Journal 41, 735-740. July 2010
Cushing’s Disease Recently(about 2 months ago) a Kaimanawa pony who was for sale and was having a vet check was diagnosed by the vet as having Cushing’s disease.This was very upsetting for the owner, and the vet should never diagnose Cushing’s disease without doing a hormone test. The owner pointed out that this was a Kaimanawa coming into winter and had never been covered in her 19 years. Although this Kaimanawa’s coat was thick and a bit wavy, this is how her coat had always been. The vet would not take this into consideration and gave a scathing report. The prospective owner decided to trust the owner and brought this lovely Kaimanawa mare. One young lady and one pony are now having fun together and hope to be on the show circuit next season. For those of you who do not know what Cushing’s disease is or the systems, below is a brief description. Cushing’s Disease in Horses Cushing’s disease or Cushing’s Syndrome, if often thought of as a disease that only affects older horses, however, it has been known to occur in horses as young as eight years old.
Symptoms of Cushing’s Disease Horses with Cushing’s Disease can be easily recognized by their coarse, wavy coat that often fails to shed out in the summer. A gelding at the barn I used to board at suffered from Cushing’s disease, and even in the heat of a Houston summer, he had a thick coat of wavy hair. Other symptoms are excessive thirst, combined with excessive urination. A normal horse will drink in the region of 5-8 gallons per day, whereas a horse suffering from Cushing’s Disease will drink as much as 20 gallons per day. Affected horses often have a pot-bellied appearance, combined with a loss of muscle on the topline. In addition, horses with Cushing’s Disease are often more susceptible to other diseases because their immune system has been compromised.
What causes Cushing’s Disease Cushing’s Disease is caused by a tumour of the pituitary gland, which is the small gland at the base of the brain which regulates the rest of the horse’s endocrine systems. As the tumour grows, it puts pressure on the nearby hypothalmus, which is what regulates the body temperature. This is believed to be the primary cause of the distinctive coarse, wavy hair coat. As cells in the pituitary gland become overactive, they excess quantities of a peptide called pro-opiolopomelanocortin (POLMC, for short) causing the entire endocrine system to go out of balance. By Jane D. Wilson
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