Il gatto Norvegese delle Foreste è una creatura fiera e maestosa, con un cuore grande e gentile, con i suoi occhi penetranti e il portamento elegante, incarna la bellezza selvaggia. È un compagno leale e giocoso, che ama esplorare e arrampicarsi. Nonostante il suo aspetto forte e robusto , è dolce e affettuoso, sempre pronto a fare le fusa accanto a te.dolcissimo con i bambini, la sua presenza calma e rassicurante trasforma ogni casa in un luogo accogliente e pieno d'amore the Character of the Norwegian Cat Until you have loved a Norwegian Cat a part of your soul will always be without light ... LOVING PROUD JOYFUL BOLD CLUMSY PARTICIPATES GOOD GARBATO STUBBORN OUTGOING ADVENTED IMPRUDENT FRIENDLY SENSITIVE PATIENT STUBBORN COMMUNICATIVE ELEGANT PRICKLY As a first note on the Norwegian Cat character I absolutely want to dispel a hard-to-die myth: " the male is more cuddly than the female or vice versa" This is absolutely false! sex does not determine the degree of affection. Often when you start looking for a cat, the question that arises is: Male or Female? It could easily happen to commit the error of relying on previous experience looking for "that affection" in the same sex as the previous cat, NOTHING MORE WRONG. You will soon realize if you come to visit me! My female cats are extremely affectionate, cuddly, outgoing, as are the males. What makes the difference is not the sex of the cat, but the time you will dedicate to interacting with her / him, obviously if you relate without prejudice, this will allow you to grasp other nuances of character, which are _cc781905-5cde-3194-bb3b- 136bad5cf58d_typical of that individual and perhaps, you will be amazed by feeling in harmony with a male, rather than a female. Being affectionate is one of the typical characteristics of this breed, both males and females alike. Who has never met him live and observes him from a photograph, due to his size, his proud appearance and his look so "feline" _cc781905-5cde-3194-bb3b- 136bad5cf58d_ may have the impression that the Norwegian Forest Cat is a detached cat .... cold ... But it will be enough to meet him live only once, to have a totally different perception and to grasp his infinite sweetness. The Norwegian cat does not meow but emits a sound similar to a trill or to the sound emitted by lynxes, it has a great ability to modulate its voice based on what it wants to express ... (we just have to find the translator! " :-D) To show us or ask for affection, the Norwegian cat invents them all, from supon a table to get to give the typical little heads, small bites, or to use his trotters to make us a caress _cc781905 -5cde-3194-bb3b-136bad5cf58d_o to touch us to attract our attention ..... _cc781905-5cde-3194-bb589094-136bad5cde-3194-bb589094-136bad5ccc3 -bb3b-136bad5cf58d_ 1_cc7819094-badd5-136bcc5_b58f5-3194-badd5-136bcc5_ -5cde-3194-bb3b-136bad5cf58d_ _cc781905-5cde-3194-bb3b-136badc5cf58d5-3194-bb3b-136bad5cf58d5 -1394c5-3194c5905-3194c5-3194c5-3194c5-3194d81-3194b905 bb3b-136bad5cf58d_ _cc7819094-badd5-136bcc5__cc7819094-5cde-136badc5-3194-badd-136bcc5_ 5cde-3194-bb3b-136bad5cf58d_ (page under construction, come back to visit us ....)

Siamo a Fornovo di Taro - Parma, potete visitarci su appuntamento. Gatti Norvegesi in Italia , mappa regione per regione. Scopri le storie dei nostri gatti in tutta Italia: link alle storie , foto e ricordi. CONTATTI DOVE SIAMO : siamo parte della "Riserva del Monte Prinzera" , nell Appennino Tosco Emiliano, tra le incantevoli vallate circostanti, in un’antica borgata a 368m sul livello del mare, a Sivizzano in provincia di Parma (Emilia-Romagna) → Scopri i nostri gatti Norvegesi in tutta Italia: Gatti Norvegesi in Italia CONTATTI : chiama per l indirizzo completo; il nostro allevamento non è un esercizio commerciale, per visitarci è necessario prenotare un appuntamento. Karin Pedrona Mobile: 389 498 4632 email: infogattinorvegesi@gmail.com

colorazione dei gatti norvegesi, silver, smoke, shaded, causati da un gene che scolora il pelo partendo dalla base, colorandolo dei toni dell argento. ( esistono 2 teorie) SILVER AND SMOKE "Il gene that makes the Norwegians shine" In some Norwegian cats the brindle design contrasts, instead of on the usual yellowish background on a background white / bright silver; in others, when they walk, the hair opening reveals the sparkle of an icy fog. These cats are always a sight e depending on the design of the coat called_bsc7905-bbc3b3-81d81-3194b9905-bbc3cc3-3194bd81-136b905-3194bd81-136bcc3 -136bad5cf58d_ (smoke), _ cc781905-5cde-3194-bb3b-136bad5cf58d_ Silver (silver), _ cc781905-5cde-3194-bb3b-136bad5cf58d7_Shaded5-136bad5cf58d_Shaded5-136bad5cf58d_Shaded5 Whatever name they are given, they all have one feature in common: the presence of a gene that makes the pigment at the base of the hair disappear completely, the area closest to the skin of cats where the hair is already normally less densely colored due to the effect of body heat on the melanin granules. The gene in question is dominant, and is indicated with the letter "I" capital Smoke, Silver and Shaded obviously can exist on all colors of Norwegians. Below you will see a large gallery of images. SMOKE: Cats are called "Smoke" in which the "I" gene, which discolours the hair at the base, is present on a "NOT TIGERED" cat The root of the hair (from 1/3 to half of the length) is silver white, while the rest is colored: the stationary cat seems to be solid in color, only when it moves can you see the contrast at the base of the hair. Often one can notice a gray shade of the black fur which forms a rich silver colored ruff. Smoke puppies often have a brindle pattern (phantom brindle), which usually disappears within the first year of life. SILVER Cats are called Silver in which the "I" gene that discolors the hair at the base is present on a "TIGRATO" cat The tab design which often includes darker and lighter bands, usually yellowish, in the presence of the silver gene, _cc781905-5cde-3194-bbcfb-136d of a very bright ice white, on which the design will stand out in a particular way. Often on puppies, up to the age of 5/6 weeks is not easily recognizable. Photo gallery of SMOKE cats with and without white Photo gallery of SILVER cats with and without white Hints of Genetics Feline genetics: a combinatorial approach Massimo Picardello University of Rome “Tor Vergata” Department of Mathematics 00133 Rome, Ital y The silver colors (smoke, silver). We now turn to the silver-colored varieties: smoke, silver tabby, shaded silver and chinchilla (and their pheomelanistic equivalents, sometimes called cameo). In these varieties, the base of the hair is depigmented, silver white, without traces of reddish tones. In some silver tabbies, however, the color reaches the root of the hair in the brindle areas. Silver tabbies are brindle cats whose agouti areas are a livid silver hue, with high contrast to brindle. Chinchillas have no traces of branding (in the case of an ideal specimen), and only the tips of the hair are colored (tipping). In shaded, the color on the tips of the hair covers about one third of the length (often less). In the smoke, the silver part is between a third and the initial half of the hair, the rest is colored. The one-gene theory In the past, a single main gene, , was considered responsible for silver colors. indicated with I (inhibitor), responsible for the braking action on the production of pigment and also for the elimination of the reddish shades typical of eumelanistic colors, especially in the agouti areas of brown tabbies. The mechanism by which a single gene can produce such different color varieties is as follows. Smokes are non-agouti cats, and the I gene lightens and bruises the base of the coat, giving it a pure silver color, evenly over the whole body. The braking action of the pigmentation produced by this gene can be limited to about a third of the hair, or be greater, reaching the middle of the hair or slightly beyond. All other silver varieties are agouti. Chinchillas and shaded are agouti with a ticked pattern. (Important warning: Chinchilla or shaded silver puppies often display a mackerel or classic [= blotched] phantom pattern, which disappears as they grow. This does not mean that these puppies are not genetically ticked. Ghost bands are common in ticked puppies: ad for example, they are sometimes seen in the Abyssinians. At most, the presence of phantom stripes may be an indication that the cub is heterozygous for the ticked pattern, but this is not necessarily true). Gene I lightens the base of the hair, but without its effect the hair would not have been all pigmented: there would have been various agouti bands, lighter. The action of I brightens the brown tones of these bands and transforms them into silver as well. Since the lightening due to the inhibition at the base combines with the further silvering of the agouti bands above the cut level of the inhibitory action, the percentage of silver hair extends, and reaches about two thirds in the case that the gene I operate in a mild way (shaded silver), and on all the hair except the tip (the last band of color of the ticked hair) in case the action of I is accentuated (chinchilla). That the chinchilla and shaded silver of eumelanistic colors are agouti is also clear from the fact that the skin of their nose is brick red (or deep pink) with the typical external border of brindle. Finally, the silver tabbies are brindle with a classic (blotched) or mackerel / spotted pattern. it is clear that the action of gene I is much more visible on the agouti areas than on the markings of the brindle, and this gives rise to the brindle design with very high contrast. But just by examining the silver tabbies we see that the genetic explanation of silver colors cannot be based on a single gene. In fact, if this were the case, the brindle markings should be lightened at the base, as in the smoke. But if on the one hand we see silver tabbies of this type, on the other hand we see many others in which the color reaches the root in the brindle areas. Geneticist Roy Robinson, in his well-known book Genetics for Cat Breeders (Cambridge, 1972, 2nd edition), suggests that on brindle areas the action of color filling overpowers silver lightening. But this seems strange, given that on smoke, where the same action occurs on the whole body, the opposite occurs. In any case, it would not be possible to explain why in some silver tabbies there is basic lightening in the brindle areas and in others not. The two-gene theory The most modern theories - see the articles by J. Jerome, TICA Trend vol. 13 n. 6 (Dec. 1992 / Jan. 1993) pg. 14 and TICA Yearbook 12 (1991), pg. 218- assert that two distinct genes act on silver, one responsible for the inhibition of the pigmentation at the base of the hair, the other for the elimination of reddish tones (bleaching, bleaching). We will call this second gene the "silver gene" (Sv). The inhibition gene, on the other hand, we will indicate with I, warning the reader on the fact that some recent texts denote with Sh the mild form of the inhibition gene, responsible for the shaded mantle, and with Ch the intense form, responsible for the chinchilla mantle . But there is insufficient evidence that the difference between the two effects is due to two alleles of the inhibiting gene rather than the action of a group of supporting polygens, and indeed the transition from shaded to chinchilla mantle is quite gradual. than net. Therefore we will not refer here to the alleles Sh and Ch, confident that the reader can now easily adapt the conclusions to the context of articles or books that instead refer to them. Therefore, in these notes we do not distinguish genotypically shaded silvers and chinchilla, attributing the difference to secondary polygens. At this point, the correspondence between the color varieties seen above and their genotypes is clear: Smoke: aa I- Sv - Shaded silver and chinchilla: A- TaTa I- Sv - Silver tabby mackerel / spotted: A- TT I- Sv - if the root of the hair in the brindle areas is silver (silver tabby shell or shaded, depending on whether the silvering is accentuated or reduced); branding is not silver. Silver tabby classic (blotched): A- TT ii Sv - if the hair root in the areas of A- tbtb I- Sv - if the root of the hair in the brindle areas is silver (silver tabby shell or shaded, depending on whether the silvering is accentuated or reduced); branding is not silver. A- tbtb ii Sv - if the hair root in the areas of We have indicated the ticked design gene in shaded and chinchilla as homozygous because the dominance of the design genes is only partial. For example, the TaT combination produces a hybrid design, with diffuse ticking partially superimposed on a mackerel design (mainly on the legs and tail, but often a little also on the flanks). If this is the genotype, the uniformity of the tipping is lost. Of course, cats with these characteristics would still be registered as shaded or chinchilla, but their color would be less consistent with the standard. It should be noted that an ideal silver tabby does not need the action of the inhibition gene I to achieve a perfect contrast between base areas and stripes. In fact, the silver Sv gene lightens and transforms the agouti bands of the hair in the base areas into a pure silver color, which therefore results silvery and livid. Furthermore, the absence of the shading gene I causes the brindle areas to be intensely colored up to the root, increasing the contrast, especially on black silver tabbies, where the elimination of reddish tones makes the black color more intense. is alive. Other color varieties predicted by the two-gene theory; the golden If we substituted genotype I- with genotype ii in shaded and chinchilla, we would obtain A- TaTa ii Sv-. Phenotypically, these cats should be silver ticked tabby in the variant ii, not shaded, that is, with a black band at the beginning of the hair, in contact with the skin. However, it does not appear that these cats were ever produced (see below for further comments). Similarly, if you do the same in the smoke, you get aa ii Sv-, which phenotypically corresponds to solid cats but without traces of rufousing, that is, reddish shades of the hair in eumelanistic colors, or warm tones in pheomelanistic colors. These cats can be obtained by crossing silvers heterozygous for the I gene. If cats of this type are then further crossed with each other, kittens of genotype ii sv sv can be born. From a line of smokes (non-agouti), normal solids are obtained in this case; from a line of shadeds or chinchillas, let's say homozygous agouti AA TaTa, normal ticked tabbies are obtained (like the Abyssinians; however all the shaded and chinchillas are selected against rufousing, that is in favor of polygens of redness of the hair that favor the more bruised, and therefore cannot be expected to obtain, from shaded parents or heterozygous chinchilla Ii Sv sv, ticked tabby puppies with warm reddish tones of the Abyssinians). But if instead shaded or chinchilla heterozygous for Sv and the inhibitor gene I are crossed, it will be possible to obtain puppies with the I-sv sv genotype. These puppies will be ticked tabby with the base of the hair lighter, but without the bruises produced by the sv gene (but still with not too bright reddish tones, due to the polygenic selection against rufousing). The base shade will be gold instead of red. This variety of color, in the eumelanistic versions, is called shaded golden. The corresponding pheomelanistic varieties are too close in phenotype to red (or cream) ticked tabbies to be classified as a variety in their own right. Similarly, golden tabbies can be obtained by crossing silver tabbies heterozygous for the Sv gene. Here are the genotypes of golden, compared to those of brown tabbies: Shaded golden and chinchilla golden (golden shell): A- TaTa I- sv sv Golden tabby mackerel / spotted: A- TT I- sv sv (note that the root of the hair in the brindle areas is depigmented: golden tabby shell or shaded, depending on whether the depigmentation is accentuated or reduced); Brown mackerel / spotted tabby: A- TT ii sv sv (the root of the hair in the brindle areas is not depigmented.); Golden classic (blotched) tabby: A-tbtb I-sv sv (note that the root of the hair in the brindle areas is depigmented: golden tabby shell or shaded, depending on whether the depigmentation is accentuated or reduced); Brown classic (blotched) tabby: A- tbtb ii sv sv (the root of the hair in the brindle areas is not depigmented.). Unverified predictions of the two-gene theory The reader must be warned that this genetic pattern is not entirely satisfactory. In fact, from it we deduce the existence of phenotypes not observed so far. For example, the aa I-sv sv genotype should correspond to a "golden smoke", ie a smoke with a base color of gold rather than silver. But to date, a cat with the color of golden but non-agouti has not been produced. Therefore, it may be assumed that the sv gene is inactivated on non-agouti cats. In this case, the genotypic difference between solid eumelanistic cats with or without traces of rufousing would be due only to the action of polygens. As already observed, also for the silvers (not golden) there is a dubious phenotype: the one corresponding to the genotype A- TaTa ii Sv-. It should be silver cats but not shaded, that is without depigmentation at the base, and with ticked design. As already observed, under the action of gene I the agouti bands become silver, and for example it is possible to see the effect of multiple alternating silver and black bands in the agouti areas of the black silver tabbies mackerel or blotched not depigmented at the base. But in case the design is ticked, we should have a phenotype with all the fur with alternating silver and black bands, and black at the base (in case the base color is black, of course). It is not known that cats of this type were ever produced. It can perhaps be assumed that the Sv gene is active only if gene I is active, and in fact it modifies and reinforces its action. The two additional assumptions we have made in this section in order to "rescue" the two-gene theory are equivalent to assuming that the entire Sv / sv allelic series is inactive except if gene I is present. No research has been done yet. experimental enough to confirm this conjecture. The theory of the golden factor If this last conjecture is true, in fact the two-gene theory becomes equivalent to another genetic model, which was introduced before the theory based on two independent genes. In this previous model, golden were explained by introducing, however, an additional gene g, whose epistatic action causes golden color instead of silver at the base of the silver coat (as is done to explain the Maltese dilution starting from gene B, with the addition of an epistatic gene d). The dominant allele G has no effect (does not cause a golden color at the base). Finally, it should be noted that the Sv gene causes a lack of rufousing in eumelanistic colors, but much less in pheomelanistic ones. There are red smokes and red shaded silvers whose tipping is quite hot red (especially in smokes). The golden theory = brown ticked tabby Another genetic scheme that was considered consisted in identifying the golden ones with simple cats of ticked tabby color (whose design is ticked all over, without any stripe of brindle; in TICA it is called "agouti tabby"). In fact, because the color of the coat is sensitive to temperature, it is almost always true that ticked tabby cats have a lighter coat base (open the coat of an Abyssinian!), And often the golden and ticked tabby phenotypes are difficult. to distinguish. Faced with the difficulties indicated above, deriving from the two-gene model of silver colors, this simple conjecture that golden is nothing other than ticked tabby is suggestive. In fact, the only phenotypic trait that this theory does not explain is the fact that some ticked tabbies are not very clear at the base while others (the golden ones) are very clear, but perhaps the difference could be attributed to the action of a group. of modifier polygens. Despite the difficulties, however, we will continue the discussion based on the two-gene theory, because it gives the most satisfactory explanation for the existence of two types of silver tabbies: those with black tabby areas up to the root and those with depigmented tabby areas. at the base of the hair. However, we observe that, as regards the most important phenotypic traits, this theory that identifies golden with ticked tabbies provides the same percentages of probability for crosses as the two-gene theory. The Broadband Gene Theory Finally, alternative theories have recently been considered in which two genes appear, but with different effects from what has been said above (contributions by H. Lorrimer on the Internet Fancier's List, March-April 1995). In fact, one gene is still the silvering (rufousing elimination) silver gene, but the other would be a gene that causes broadening of the light bands in agouti hair, called wide-band (Wb). However, it should be noted that, due to the large degree of variability in the length of the tipping, it would be more appropriate to speak of a group of broadband branding polygens. In this theory, the problem related to the fact that golden are only agouti (golden smokes are not observed) is obviously solved, but on the other hand the smokes are not explained, which are not only silver (i.e. without rufousing), but also lightened at the base. As these are non-agouti cats, this aspect of their phenotype cannot be due to genes that widen the clear agouti bands. On the other hand, a variant of this theory can be used to justify a theory advanced in some books: that chinchillas and shaded silver are not necessarily of ticked design. The ticked design, together with the silver inhibiting action, ensures that the color is limited to the tip of the hair (tipping). For g | the other designs this would not be the case, and furthermore the length of the tipping would be far from uniform. But if the agouti bands were dilated by a group of wide-band polygens, and then silvered by the silver gene, then the tipping would be confined to the tip of the hair, and there would be an acceptable degree of uniformity. The theory [golden = brown ticked tabby + broadband polygens]: finally an exhaustive genetic model for smoke, silver and golden! Let us return to the theory that identifies the shaded golden and ticked tabby color varieties. This is 19 the most satisfactory theory we have encountered, except for the crucial circumstance which does not explain the partial depigmentation at the base of the hair, a fundamental characteristic of the shaded golden phenotype. On the other hand, there are many cats registered as golden and with varying degrees of depigmentation, some even with almost no depigmentation ... Therefore it must be assumed that shaded golden depigmentation is not the effect of a main gene with net action. (or depigmentation or full color), but the result of the gradual (and sometimes very reduced) action of a set of polygens. But there is already a candidate for this group of polygens: the broadband modifiers introduced in the previous section. Then shaded golds would be nothing more than ticked tabby with broadband base brightening (aside from eye color, which we'll talk about later). If so, everything is fine: the golden must be tabby (no golden smokes!) And partially depigmented at the base (but the amount of depigmentation varies from one specimen to another depending on how much the effects of the individual modifier genes are added together. broadband). Naturally, in this theory the ideal shaded golden results result from crosses of shaded silver heterozygous for the silver and homozygous for the ticked pattern. What if the shaded silver parents are heterozygous also for the ticked drawing? For example, parents might carry the mackerel factor. In this case, if instead of being silver they were brown tabby (no silver), the parents would have brindle lines on the legs, chest and tail, due to the partial dominance of the ticked allele on the mackerel. But as they are shaded ilver, the branding lines will be there, but they will be faint. And in fact, there are some shaded silvers with faint traces of branding (especially from puppies, before the agouti gene reaches maximum effect). However, their golden kittens are not silver, they are brown ticked tabby, and if they carry the mackerel allele the bruises will be clearly visible on the paws, a very undesirable feature in shaded golden, but frequent. To complete the picture, the broadband modifiers transform the other designs (spotted, mackerel and classic) into the corresponding golden varieties (golden spotted tabby, golden mackerel tabby and golden classic tabby respectively), in which the agouti areas are partially depigmented at the base and have warm apricot tones. Now we finally have a satisfying golden theory. However, in order to be compatible with the silver one, it is necessary to review and correct the latter. We can no longer hypothesize two genes for silver, one for depigmentation and the other for silvering. Instead we have to go back to the one-gene theory, an inhibitory gene that we will continue to call I and that simultaneously causes silvering and depigmentation, as in smokes, for example. It should be noted that the golden genotype is not due to gene I (indeed the golden ones are heterozygous ii): the depigmentation at the base of the golden hair is instead due to the elongation of the first agouti band due to the action of the broadband modifier genes. We do not introduce a distinct main gene that causes depigmentation, otherwise, as we have seen, the theory would predict the non-existent golden smokes (golden non agouti, depigmented at the base of the hair). On the other hand, it would seem at first glance that this loses the brilliant explanation that the two-gene theory gave regarding the fact that some silver tabbies are depigmented at the root of the hair in the brindle areas and others are not. But this genetic trait can be explained in some other way. The gradual level of depigmentation at the base of the hair in the brindle areas may be caused by modifier genes similar (or possibly identical) to broadband modifiers, whose action is limited to tabby cats. With a slight conceptual abuse we can imagine that these additional modifiers belong to the same group as the broadband polygens (in reality this is not the case, because the latter act on the agouti base areas while the former act on the brindle areas: but in reality they meet many golden in which broadband depigmentation also occurs on the areas of tabby marks ...). In summary, compared to the two-gene theory our new genetic model retains the inhibitor gene I (which is now considered responsible for both depigmentation and silvering, as in the one-gene theory), and replaces the second gene with a group of polygens. , which we will denote by Wb (for "wide-band"). What is particularly satisfying is the fact that the gradual action of broadband modifiers can explain the difference between the shaded silver and chinchilla phenotypes. Unfortunately, however, we are assuming that these are polygens, which therefore are not subject to the simple and direct rules of Mendelian genetics for the main genes. In order to analyze the mathematics of this new model it is necessary to resort to statistics, the results of which are too fine to be clearly distinguished in the phenotypes. Therefore it is not easy to present the results by means of cross tables. Silver and golden It should be noted that the deepening of the single gene theory presented in the previous section, as well as the variant introduced previously, excludes the possibility of cats at the same time silver and golden: the silver phenotype is a consequence of the inhibitory gene, which the golden they do not have. Both shaded silver and golden have broadband type color suppression or lightening genes, or polygenic modifiers of the same type. In the latest version of the theory that we presented immediately above, the golden pattern is caused by the suppression action of this type of genes superimposed on hairs with already banded coloring due to the Agouti gene: thus, if the tabby design is the ticked, you get the perfect golden pattern, uniform throughout, but if the design is mackerel, spotted or (even worse) blotched, then more or less large areas of tabby marks become evident with full color, not very lightened, only orange in color in the band at the base. These patterns could be classified as golden tabby (mackerel, spotted or blotched, respectively). Since in such cases the areas where the coat has a broad golden base are less broad, these phenotypes are more difficult to determine with certainty, particularly in kittens, especially if they are phantom patterns in young cats due to heterozygous tabby genotypes with a only ticked allele, and some origins books (for example that of TICA) do not recognize them. Finally, it should be noted that the action of broadband suppression genes creates long agouti bands of pheomelanistic color, which are difficult, if not impossible, to recognize on cats of already pheomelanistic base color. If the lightening band is not long this is easier, just like in the case of the tortie ticked tabby pattern. Eye color of shaded and golden: an example of persistence? In relation to the similarity between golden and ticked tabbies, it should be remembered that in ticked tabbies the color of the eyes is gold or copper (in the case of Persians) or also hazel or yellow or yellow-green or green (in the Abyssinians). In the shaded silver or chinchilla of eumelanistic colors the eye color is not gold or copper, but emerald or blue-green. Instead, in the shaded silver or chinchilla of pheomelanistic colors, the eye color is copper. With appropriate crossings and consequent selection, it has been possible to introduce the gold or copper color in the eumelanistic shaded silver: the corresponding standard, recognized by some feline associations but not all, is called black shaded (in England, pewter). So the difference between an eumelanistic golden and the corresponding ticked tabby, although it may be barely visible in the color of the hair, is still evident in the color of the eyes, emerald in the first but not in the second. In silver tabbies, on the other hand, the eyes are green or yellow-green or gold, with a preference for green. In the shaded and in the pheomelanistic silver tabbies the color of the eyes is copper, and in the corresponding tortoiseshell varieties it can be copper or emerald (shaded) or green (silver tabby), with preference for copper. The existence of black shaded with gold eyes reveals that the emerald color of the eyes is not caused by the silver gene. It is interesting to observe that, although the color of the eyes, emerald or copper, is largely determined by a main gene, it is not common to meet eumelanistic shaded silvers with copper eyes: the emerald color occurs more frequently. So, although the color of the eyes and the hair depend on different genes, somehow there is a persistent link between the shaded silver coat and the emerald color of the eyes. This link is perhaps due to the fact that the main genes that cause this eye coloring are located on the same chromosome as the genes that cause the shaded silver color of the coat, and therefore the genetic transmission of one and the other occurs together. A situation of this type, which is called persistence, modifies the probabilities of concomitant genetic transmission of the two genes, which are very different from what they would be for two independent genes. To break the persistence, in fact, it is necessary that in the close contact of the two homologous chromosomes during the pairing that precedes meiosis, a genetic recombination takes place, that is a molecular exchange between the two chromosomes. The action of the I and Sv genes is epistatic on that of the solid color, eumelanistic and pheomelanistic genes, but not on that of the white (W) and piebald spot (S) genes. Obviously, the W- B- A- TaTa I- Sv- genotype corresponds to a phenotype in which white masks the shaded silver color on the coat, but the eye color can be either blue (due to the depigmentation action that the gene W can exert on eye color) or emerald.

Maschi del nostro allevamento amatoriale di gatti norvegesi, vivono in casa e nei catrun ( recinti protetti) - Non sono disponibili per monte esterne- father: NO * FRU PEDERSENS PEDER STARUP mother: SE * ZYGOT ALLEY-OOP NO * Fru pedersen ISAK SYLVESTER Blood Type A 1st scan HCM -Negative Oct. 2015 2nd scan HCM -Negative Nov. 2017 3rd scan HCM -Negative June 2019 4th scan may 2021 - Negative PKD-PK Def - GSD4: Negative Fiv Felv: Negative 2019 Chlamydia: negative Aug. 2019 HerpesVirus Negative Aug. 2020 CalciVirus Negative Aug. 2020 Blood Type A 1st scan HCM -Negative Oct. 2015 2nd scan HCM -Negative Nov. 2017 3rd scan HCM -Negative June 2019 4th scan may 2021 - Negative PKD-PK Def - GSD4: Negative Fiv Felv: Negative 2019 Chlamydia: negative Aug. 2019 HerpesVirus Negative Aug. 2020 CalciVirus Negative Aug. 2020 father: NO * FRU PEDERSENS PEDER STARUP mother: SE * ZYGOT ALLEY-OOP NO * Fru pedersen ISAK SYLVESTER Blood Type A 1st scan HCM -Negative Oct. 2015 2nd scan HCM -Negative Nov. 2017 3rd scan HCM -Negative June 2019 4th scan may 2021 - Negative PKD-PK Def - GSD4: Negative Fiv Felv: Negative 2019 Chlamydia: negative Aug. 2019 HerpesVirus Negative Aug. 2020 CalciVirus Negative Aug. 2020 father: NO * FRU PEDERSENS PEDER STARUP mother: SE * ZYGOT ALLEY-OOP NO * Fru pedersen ISAK SYLVESTER Blood Type A 1st scan HCM -Negative Oct. 2015 2nd scan HCM -Negative Nov. 2017 3rd scan HCM -Negative June 2019 4th scan may 2021 - Negative PKD-PK Def - GSD4: Negative Fiv Felv: Negative 2019 Chlamydia: negative Aug. 2019 HerpesVirus Negative Aug. 2020 CalciVirus Negative Aug. 2020 Blood Type A 1st scan HCM -Negative Oct. 2015 2nd scan HCM -Negative Nov. 2017 3rd scan HCM -Negative June 2019 4th scan may 2021 - Negative PKD-PK Def - GSD4: Negative Fiv Felv: Negative 2019 Chlamydia: negative Aug. 2019 HerpesVirus Negative Aug. 2020 CalciVirus Negative Aug. 2020

il Pedigree è la carta di identità del gatto, non un titolo nobiliare. E' l unico strumento che vi assicura che l' allevatore ha rispettato regole rispetto al benessere delle madri... the pedigree If they want to sell you an IPHONE and tell you it's new, the latest model, NEVER USED he !! MAoooops! _Cc781905-5cde-3194-bb3b-136bad5cf58d_ ...._ cc781905-5cde-3194-bb3b-136bad5cf58d_ is without box! .... without receipt ... and they ask you € 150 ...._ cc781905-5cde-3194-bb3b-136bad5cf58d_ COMES THE DOUBT THAT SOMETHING IS WRONG ??? ....._ cc781905-5cde-3194-bb3b-136bad5cf58d_ WELL, the pedigree of the cat, this elusive sheet of paper, is none other than the cat's identity card, which, as for human beings, is issued by an association entitled to do so (ANFI) and recognized by the Italian State, where you will see written who are the father the grandparents, the great-grandparents, etc. You could easily think, but what interests me ???? I'm interested in the cat ... why do I have to spend 1000 euros to get a sheet of paper when with 200-300-400 euros I can still have a Norwegian? I will try to explain it to you as clearly and as briefly as possible. You are about to be simply cheated! _Cc781905-5cde-3194-bb3b-136bad5cf58d_ What does the word "pedigree" mean click here : A PEDIGREE COSTS BETWEEN 13 AND 20 EUROS SEE ANFI RATES (see Genealogical Certificate within 6 months of birth) http://www.anfitalia.it/site/index.php?option=com_content&task=blogsection&id=12&Itemid=53 ---------------------- Very important thing: SELLING A CAT WITHOUT PEDIGREE SPLITING IT AS "PURE" IS AN ADMINISTRATIVE OFFENSE. The pedigree is the identity card of the cat, where it is written who are the parents, it is only through the pedigree that you can prove who your puppy is from and therefore being able to say it is a "purebred" cat here is the LAW! DLG 529/1992: ART. 5 ----------------------- Having a cat that has pedigree gives you 4 guarantees: 1 l breeder giving you the puppy: did not mate the parents in consanguinity because in the pedigree this would be seen. 2 the father and mother are really 2 Norwegians of the Forests, and your puppy is not the result of crosses with cats that are clearly not purebred are not tested, checked and vaccinated. 3 there is no exploitation to the detriment of the health of female cats in that breeding. 4 the animal was born and raised in Italy; often behind the sold-out animals there is the trafficking of illegally imported specimens ... and of these there are more those who die during transport than those who come to have a master ... removed from their mothers too soon, crammed into some truck with hallucinating journeys ... diseases ...... etc ---- WORTH IT FOR A FEW HUNDREDS OF EURO continue to foment this thing? IF THERE WERE NO REQUEST THESE THINGS WOULD NOT HAPPEN! 5 The parents of the pedigreed puppy must have filed the genetic tests in ANFI that attest to the absence of some genetic pathologies. These tests are MANDATORY in order to obtain the release of the pedigree, without which ANFI does not produce them. 6 The parents of the pedigreed puppy are COMPULSORY microchipped, in this way, there is real traceability and it is possible to prove the genealogy, therefore your cat is really a descendant of the Norwegian forest cats. ------------------ 1 -What does inbreeding involve in your future puppy? these are some of the main diseases not visible at the time of purchase: Teeth alignment _cc781905-5cde-3194-bb3b94d-136bcc5-3194-bb589094-136bcc5-3194-bb589094-136b -136bad5cf58d_ Cataract _cc781905-5cde-3194-bb589094 -5904bad5c3-3194-bb589094_bad5c3-3194-bb589094bad5c5c Deafness Gangliosidosis GM1 _cc781905-5cde-3194cf58d-136bcc5-3194c5-bb58c5-3194c5-bb3badb 136bad5cf58d_ Gangliosidosis GM2 _cc781905-5cde-3194cf58d-136bcc5-3194c5-bb3-badd5-136b58c5-3194c5-bb3badb 136bad5cf58d_ Haemophilia A and B _cc781905-5cde-3194-bb3b-84c5-badd-136b58c5-3194c3b-136cc5-3194-bb3b-136b bb3b-136bad5cf58d_ Cleft lip and cleft palate _cc781905-136bad5cf58d_ _cc781905__3bcde-3194bdcc3 bb3b-136bad5cf58d_ Hyperoxaluria Patella Dislocation _cc781905-5cde-3194-bb589094-136bcc3-3194-bb589094-136bcc5__ -136bad5cf58d_ Spasticism _cc781905-5cde-3194-bb3b_ 136bad5cf and much more 2 -what involves buying a crossbred cat, which clearly cannot be vaccinated, uncontrolled with untested cats: Feline leukemia; Viral immunodeficiency syndrome or fiv and much more .... And to conclude: 3- Often, the sale of puppies without pedigree, as an excuse, hides the exploitation of the mother cat, causing her to give birth several times a year ... ANFI tries to limit the problem of the production of kittens "in battery" by imposing a limit of only 3 litters in 2 calendar years for each bitch of a breeding farm (Article 17 Breeding Regulations and Origins Books): if a cat is made to give birth more often, ANFI does not allow the registration of puppies and, consequently, the issue of pedigree. When a breeder or private vi proposes the purchase of a cat without pedigree, know that, by accepting, you are probably contributing to the exploitation of a cat in her third, fourth, fifth pregnancy in a year! And this is a practice that MUST be stopped because it jeopardizes the health of the cat but also that of the new born! IN SUMMARY FOR 100, 200,300, 400 EUROS YOU WILL HAVE ...... YOU DON'T KNOW WHAT ......_ cc781905-5cde-3194-bb3b-136bad5cf58d_ THE THING I WISH YOU IS THAT LUCK WILL ASSIST YOU AND BE AT LEAST HEALTHY, EVEN IF NOT NORWEGIAN ..._ cc781905-5cde-3194-bb3b-136bad5cf58d_ BECAUSE THIS MONEY WILL BE ONLY AND EXCLUSIVELY THE EARNINGS OF A SCAM, AND NOT THE GUARANTEE OF CARE TESTING AND SERIOUSNESS WHICH CAN GIVE YOU A FARMER.

Carne cruda per gatti: guida BARF completa ai tempi di congelamento di pollo, manzo, pesce e altri alimenti per ridurre rischi parassiti e virus." TUTTI I TESTI SONO DI PROPRIETA' DI KARIN PEDRONA -E' VIETATA L ' INTERA O PARZIALE RIPRODUZIONE DEI TESTI Natural Power La qualità inizia dal banco! 🥩 L' Acquisto Il congelamento serve soprattutto per ridurre il rischio parassitario, ma la carica batterica della carne dipende da quanto è fresca al momento dell’acquisto. Una carne appena arrivata al macellaio o al supermercato avrà meno proliferazione batterica rispetto a una che è rimasta diversi giorni nel banco o in cella frigorifera. Puoi prenotare la carne in anticipo dal tuo macellaio di fiducia o chiedere in quali giorni arrivano le nuove forniture al supermercato: così sei sicuro di congelare un prodotto con carica batterica più bassa. Ricorda: più fresca è la carne al momento del congelamento, più sicura sarà al momento della somministrazione al gatto. 👉 Non basta solo congelare: la scelta della materia prima è il primo passo verso una dieta cruda sana e sicura. ⚠️ Congelare non è sterilizzare Il congelamento non è una sterilizzazione: non elimina batteri come Salmonella o Listeria, e non è affidabile contro virus. Serve soprattutto per ridurre i parassiti (Toxoplasma, Anisakis, Sarcocystis) e fermare la carica batterica al punto in cui la troviamo al momento del congelamento Va detto in onestà che i gatti sono MOLTO più resistenti di noi ai batteri enterici, grazie all’acidità gastrica molto più forte e a un transito intestinale rapido, inoltre le patologie causate da Cryptosporidium, Sarcocystis e Toxoplasma sono molto rare. Per questo quando si fa dieta barf o si da carne cruda è sconsigliato l' utilizzo concomitante della crocchetta che rallenta il transito 📩 per sapere come fare una dieta BARF sicura ed equilibrata - Scrivimi a Karin@barfcoach.it ⏱️ Tempi di congelamento 👉 Regola generale (uso domestico): Il congelamento riduce i parassiti solo se la temperatura arriva a cuore del pezzo. I tagli più spessi richiedono più tempo. Per prudenza: imposta il freezer che scenda a –20 °C o mantieni i tempi più lunghi. Così il rischio si riduce al minimo e il tuo gatto può godere del crudo in sicurezza. 🐔 Pollo/Tacchino → –20 °C · 72–96 h 🐇 Coniglio → –20 °C · 72–96 h 🐮 Manzo → –20 °C · 96–120 h 🐑 Pecora/Agnello → –20 °C · 96–120 h (fino a 144 h se tagli spessi) 🐐 Capra → –20 °C · 96–120 h 🐟 Pesce (acqua salata) → –20 °C · 48–96 h (UE: 24 h a –20 °C o 15 h a –35 °C) 💧 Pesce (acqua dolce) → –20 °C · 7 giorni 🦑 Cefalopodi → –20 °C · 48–96 h 🦐 Crostacei → –20 °C · 48–96 h 🦪 Molluschi bivalvi → 🚫 solo cotti 🐷 Suino/Cinghiale → 🚫 solo cotti Nel Dettaglio: Pollame e Coniglio → Toxoplasma gondii Pollame e coniglio possono ospitare cisti di Toxoplasma gondii. Studi indicano che il congelamento a –12 °C per 2–3 giorni o a –20 °C per 2–4 giorni inattiva gran parte delle cisti (Alizadeh et al., 2018; Gracia et al., 2022). Per uso casalingo si consiglia prudenzialmente: –20 °C per 72–96 h. Manzo → Sarcocystis spp. e Toxoplasma Oltre a Toxoplasma, il manzo può ospitare Sarcocystis spp., parassita intracellulare più resistente. Studi recenti su ovini (Peris et al., 2024) raccomandano –20 °C per 96–144 h per eliminare le cisti. Raccomandazione pratica: –20 °C per 96–120 h. Pesci → Anisakis e altri Pesci d’acqua salata: rischio Anisakis. La normativa UE (Reg. 1276/2011) impone: –20 °C ≥24 h o –35 °C ≥15 h. In casa, meglio 48–96 h per compensare le performance ridotte dei freezer domestici. Pesci d’acqua dolce: rischio Opistorchis, Clonorchis, Diphyllobothrium. Richiedono tempi più lunghi: –20 °C per 7 giorni. Cefalopodi (seppie, calamari, polpi) Parassita principale: Anisakis. Stesse regole dei pesci: –20 °C per 48–96 h. Crostacei (gamberi, scampi, aragoste, granchi) Rischio parassitario basso, ma possibili contaminazioni da Anisakis e batteri marini (Vibrio, Listeria). Congelamento riduce il rischio parassitario, non elimina batteri. Raccomandazione: trattare come pesce → –20 °C per 48–96 h. Molluschi bivalvi (cozze, vongole, ostriche) Il rischio maggiore non sono i parassiti, ma virus e batteri accumulati per filtrazione: Vibrio, Norovirus, virus dell’epatite A. Congelamento NON li inattiva. Per l’uomo i bivalvi crudi sono un rischio documentato; per il gatto non ci sono prove solide, ma studi hanno trovato norovirus felini (FNoV) associati a diarrea nei gatti (Martella et al., 2015; Sumiyoshi et al., 2025). Vibrio è stato isolato anche in infezioni da ferita da morso di gatto, segno che il batterio può colonizzare i felini, pur senza prove forti di trasmissione alimentare. Raccomandazione: mai bivalvi crudi al gatto. Solo cotti o da fonti certificate. Suino e cinghiale → divieto assoluto Virus di Aujeszky (pseudorabbia) → sempre fatale per gatti e cani. Congelamento non è misura affidabile: il virus può resistere settimane. Regola: mai carne suina/cinghiale cruda. ✅ SALVA LE SLIDE per avere a portata di mano la tabella dei congelamenti Aiutami a continuare la mia opera di diffusione gratuita , regalami un like e un seguimi sui social! TUTTI I TESTI SONO DI PROPRIETA' DI KARIN PEDRONA -E' VIETATA L ' INTERA O PARZIALE RIPRODUZIONE DEI TESTI

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gatto maschio silver norvegese delle foreste TINGOSKATTENs JARL _cc781905-5cde -3194- bb5894_ISbad5c3 -owner WORLD'S Cattery -Milano Italy Scan Hypertrophic Cardiomyopathy Issued by Claudio Bussadori Dates 21/11/18 (age 1.4.15) Result Normal - - - RDA (PCR) Date 12/2/2019 Chlamydya- Herpes- Chalices- Mycoplasma Result Negative - - - * Pedigree * Tingoskattens Jarl, M, NFO ns 24, 06/07/17, NO / IT Father: NW SC Sakeena's Aston Martin, JW Mother: Tingoskattens Zona

Catrun gatti, recinto per gatti, costruzione del recinto, protezione finestre, protezione balconi, tettoia per gatti, pote per gatti, strutture legno recinto My CATRUNs

Qui potrai leggere e guardare video e fotografie nonchè tutte le leggende gatti norvegesi delle foreste The code of COLORS or EMS code - Easy Mind System The EMS (Easy Mind System) code is the system that the Associazione FIFè uses to identify the breed and color of cats through codes. It is a system that works with all cat breeds but we will focus on the color codes attributable to the Norwegian Forest Cat. Each breed is identified with an abbreviation of three capital letters, the Norwegian Forest Cat is indicated with NFO (Norwegian FOrest) Once the breed has been identified, in our case NFO, we have the letters indicating di what color is the cat and that is: n: black, a: blue , d: red, e: cream , _cc5c1-581e -3194-bb3b-136bad5cf58d_ g: blue cream, w: white, nt: amber, _cc781905-5cde-3194-bb3bbad : , dt: amber-based red, et: amber-based cream, ft : amber7905c -3194-bb3b-136bad5cf58d_ gt: light amber tortie After having identified the color if Il gatto is silver or smoke or golden, the letter s or y must be inserted after the color. If the cat has white according to the quantity and distribution will be indicated according to the following table : 01 van, 02 arlequin (harlequin), _ cc781905-5cde-3194-bb3b-136bad5cf58d_ 03 bicolor. 09 any quantity of white If the cat does not have white we will not find any of these indicated numbers. If the cat is brindle, then we will have the numbers indicating the type of brindle: 11 Shaded, 21 Undefined tabbing , 22 Blotched tabby (classic tabby) _cc781905-5cde-3194-bb3b81-136bbad5cf58d5-1390 tabby 3190_backer_5cf58d5 -136bad5cf58d_ 24 Spotted tabby 25 Ticked tabby And finally the color of the eyes: 61 blue, 62 arancioni / _cc79094-bad5-136cc5_arancioni / _cc7905-bad5-136 -5cde-3194-bb3b-136bad5cf58d_ 63 unequal eyes, 64 green three colors blotched with white - f0322 three colors with white - f09 tortie blotched f22 tortie f tortie mackerel with white f0323 tortie mackerel f23 three colors harlequin f02 tortie smoke fs blue cream with white g09 blue cream (ems: g)

La salute dei Gatti Norvegesi non viene lasciata al caso...Siamo seguiti da Veterinari specializzati... 🧬 GARANZIE SANITARIE COMPLETE 2025 Test Genetici + Virali + Respiratori TUTTI NEGATIVI • CERTIFICATI LABORATORIO Our Veterinarians, Specialists and analysis laboratories Pyruvate Kinase Deficiency (PK-Def) Pyruvate kinase deficiency (PK-Def for short) is a genetically based disease. Pyruvate kinase is an enzyme found inside red blood cells and controls their ability to produce energy to survive. When the enzyme is deficient, the red blood cells undergo premature destruction (erythrolysis) and this therefore leads to a reduction in their blood number. The resulting anemia is therefore the primary consequence of the deficit. However, the diagnosis of PK-Def on a symptomatic basis can be very difficult: since the cat's body is able to adapt the production of red blood cells in the face of their decrease, anemia can occur occasionally or intermittently. The development of the disease is slow, in most cases, with vague symptoms such as lethargy and loss of appetite. However, there is the possibility that the cat will develop very severe anemia, which could put its survival at risk. PK-Def is a congenital disease with a genetic basis, for which there is no cure and, since anemia is very often mild, the clinical signs may not be immediately obvious and therefore the condition may be underestimated for a long time. There are cases of deaths within two years, but also cases where the life expectancy is long (over 8 years). It is essential for a cat affected by the disease that its living conditions are optimal and that stressful events are avoided as much as possible. The disease is typical of the Abyssinian and Somali breeds, but can be found in breeds that have undergone hybridization with the Abyssinians or Somalis as well as in domestic cats. Genetic profile PK-Def is an autosomal recessive disease. This means that a cat can be defined: normal: does not have any copy of the defective gene, will not become ill with the disease or pass the disease to the offspring carrier: in the pair of alleles that define the disease, there is a defective allele. The cat will never get sick, but it will be able to pass the mutation to the offspring affected: the pair of alleles is composed of two defective chromosomes. The cat will develop the disease and will certainly pass the mutation on to the offspring. In case of mating between two PK-Def carriers, since both parents have a copy of the defective gene, they will be able to pass the mutation to the offspring. Specifically, two carriers will generate 25% of puppies affected by the disease, 50% of carrier puppies and 25% of healthy puppies. In case of mating between a carrier cat and a healthy cat (ie not a carrier of the deficiency), we will have 50% carrier cats and 50% healthy cats. In a mating between two affected cats, 100% of the offspring will be affected. Management on the farm From a breeding point of view, affected cats should not be used for breeding. It is possible to use carrier cats, obviously defining a control and negativization plan of the line, to manage the pathology as much as possible and go towards the eradication of the pathology in the breed. In the Abyssinian and Somali breeding, due to the small number of subjects currently working with, the breeding plans include the conscious use of carriers, because their carpet sterilization would involve serious problems of numerical consistency of the gene pool. In general, what needs to be done when deciding to use a carrier on the farm is to mate it with non-carrier cats, test the litter and prefer to continue working on the line keeping mutation-negative cats on the farm. In this way, the dual objective of "cleaning" the bloodline and, at the same time, of preserving it will be achieved. The UC Davis study As we have already published in the previous article, News on PK-Def in Norwegian Forest Norwegian, un recent study by UC Davis_cc781905-5cde-3194_badica-136b3b the disease is also present in the Norwegian Forest Cat, although at present we do not yet have precise indications on the gene frequency and on the consequent percentages of carriers and affections in the breed. We therefore suggest, in this first phase, to test your cats and to submit the results of the tests to the public databases for collecting the results, to allow a more in-depth study on the spread of the mutation. Where to take the test Since the mutation found in the Norwegian Forest Cat is the same as the one found in the Abyssinians and Somalis for which genetic testing already exists, it is possible to test your cats in different laboratories that are already certified to perform the test. It is possible to perform the test with either a blood sample or a buccal sample. Here is a non-exhaustive list of the laboratories to which you can turn: Genefast (Italy - agreement with Anfi) Vetogene (Italy) UC Davis (USA) Laboklin (Germany) Text taken da http: //www.clubnorvegesi.com/ Type IV Glycogenosis GSD IV (glycogen storage disease type IV) is part of a group of diseases, called glycogenoses. Type IV affects the Norwegian Forest Cat. They are well described pathologies also in humans, classified as rare diseases. In a normal organism, the excess glucose obtained from the diet or from the conversion of proteins and fats is stored in a branched chain of polymers, glycogen, built using the enzyme GBE (glycogen branching enzyme) as a catalyst. When the body needs energy, glucose molecules are removed from the glycogen and released into the bloodstream or used by the tissues. The ability to efficiently add and remove glucose from glycogen depends on the complexity of its branching structure. GSD IV is a hereditary deficiency of the GBE enzyme: affected subjects store an abnormal form of glycogen which, therefore, leads to an insufficient use of glucose. Hence GSD IV can be considered a chronic hypoglycemia that inexorably worsens towards death (because the body is unable to use glucose effectively). In cats, affected kittens die a few hours or days after birth, most likely because they do not have enough glucose to survive delivery and the first hours / days of life. The late form is rarer, for which the puppy is healthy up to 5/7 months and then suddenly shows a stunted growth and widespread weakness, with the following symptoms: high hyperthermia (over 40 °), insensitive to corticosteroids intermittent and generalized tremors that become permanent intermittent, "hiccup" weakness muscle weakness, followed by muscle atrophy, fibrotic contractures of joints that lead to movement and feeding difficulties and that require continuous assistance from the owner quadriplegia Affected cats can survive up to 10/14 months. They die of cardiac arrest, sometimes after coma. The disease is fatal and there is no cure. It is possible that it is confused with neonatal isoerythrolysis because the symptoms can suggest both pathologies. The only thing that can be done is the test (genetic for GSD IV, blood group identification with B allele typing for neonatal isoerythrolysis). Genetic profile The GDS IV mutation is recessive, which implies that the possibility of it expressing itself in the offspring exists only if both parents are carriers of the mutation. There are 3 different possibilities: both parents are healthy (they are homozygous for the normal allele): the children are healthy and will not carry the mutation. if one of the parents is carrier (heterozygous) we will have about 50% carrier and 50% healthy cats among their offspring. When two carriers are mated we get 25% sick cats, 50% carriers and 25% healthy cats. Recall that a carrier cat is a cat that does not have the disease and that will never develop it. However, he will be able to to transmit the mutation to his children. The test A genetic test, on blood or buccal swab, is available to identify not only affected cats but also carriers. Some laboratories that perform this test are: Vetogenic Genefast Antagen Genindexe Laboklin PennGen Each laboratory provides for the sending home, upon request, of the test material (swabs or blood collection tubes), together with the necessary documentation. In some cases it is required, for a correct identification of the cat, that the microchip is applied. Insights FYFE et al. (2007) A complex rearrangement in GBE1 causes both perinatal hypoglycaemic collapse and late-juvenile-onset neuromuscular degeneration in glycogen storage disease type IV of Norwegian forest cats, Mol Genet Metab. 90, 4, 383-92. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17257876 Glycogenoses on Wikipedia FYFE et al. (1992) Glycogen storage disease type IV: inherited deficiency of branching enzyme activity in cats., Pediatr Res. 32, 6, 719-25.FYFE (1995) Glycogen storage disease in cats, J Am Vet Med Assoc. 206, 3, 286. GASCHEN et al. In Congenital feline myopathies, Glycogen Storage disease type IV, 360-361 http://www.winterfyre.com/testing/ http://gsd4.de.vu/ v Text taken da http: //www.clubnorvegesi.com/

Esposizioni, show, mostre, carriere espositive... Perché nel mio allevamento non partecipiamo alle esposizioni Le esposizioni feline rappresentano momenti importanti per molti allevatori: permettono di condividere la passione, confrontarsi con altri appassionati e valorizzare le caratteristiche della razza. Nel mio allevamento, ho scelto invece un percorso differente, guidato dal principio dell’allevamento etico e dalla consapevolezza dell’antropocentrismo. Questo concetto ci ricorda quanto spesso le decisioni vengano valutate secondo il metro umano, dando più peso a immagini, standard e risultati visibili rispetto ai reali bisogni dei gatti. La mia priorità è garantire il benessere quotidiano dei Norvegesi delle Foreste, permettendo loro di vivere serenamente, esprimere i comportamenti naturali e crescere in un ambiente stimolante, sicuro e tranquillo. Per me, un Norvegese delle Foreste è davvero bello quando è sereno, equilibrato e felice, non quando è stressato, strapazzato o esposto a stimoli innaturali. La bellezza non è solo estetica, ma il riflesso di un benessere reale: occhi vivaci e atteggiamenti armoniosi nascono da libertà, cura e rispetto dei bisogni del gatto. Non si tratta di giudicare chi partecipa alle esposizioni. È una scelta personale, legittima e rispettabile I rischi della corsa alla perfezione Negli allevamenti e nelle esposizioni si crea spesso un circolo vizioso: la bellezza premia l’estremo, e l’estremo mette a rischio il benessere. Lo abbiamo già visto nei , nei cani e gatti brachicefali come i Persiani. È come una scala che si alza gradino dopo gradino: ogni piccolo miglioramento estetico viene applaudito, ogni tratto accentuato diventa desiderabile e chi si ferma rischia di restare indietro. Allevatori e giudici, pur amando sinceramente i gatti, iniziano a valutarli secondo i criteri umani di perfezione, non secondo i loro bisogni reali. Il gatto diventa un “progetto estetico” una figura geometrica a cui assomigliare In questo modo, la competizione e l’ossessione per l’aspetto generano sofferenza invisibile: premi e lodi rinforzano comportamenti e scelte che stressano l’animale, fino a trasformare un gatto naturalmente bello in un essere sofferente, pur senza cattive intenzioni.