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		<title>Babesiosis in dogs</title>
		<link>https://labogen.com/en/2026/03/10/babesiosis-in-dogs/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Tue, 10 Mar 2026 11:07:07 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<guid isPermaLink="false">https://labogen.com/2026/03/10/babesiosis-in-dogs/</guid>

					<description><![CDATA[Babesiosis in dogs &#8211; Invisible danger after a tick bite Babesiosis (also known as &#8220;canine malaria&#8221; or piroplasmosis) is a disease caused by unicellular parasites (babesia) that dogs can get from the bite of infected ticks and is increasingly occurring in Germany. It is mainly transmitted by the meadow tick and the brown dog tick, [&#8230;]]]></description>
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							<h2>Babesiosis in dogs &#8211; Invisible danger after a tick bite</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>Babesiosis (also known as &#8220;canine malaria&#8221; or piroplasmosis) is a disease caused by <strong>unicellular parasites (babesia) </strong>that dogs can get <strong>from the bite of infected ticks</strong> and is increasingly occurring in Germany. It is mainly transmitted by the meadow tick and the brown dog tick, and more rarely by blood transfusions. If the parasites enter the dog&#8217;s bloodstream, they penetrate the red blood cells and multiply there. This destroys the red blood cells, which leads to <strong>anemia</strong>.</p><p>The <strong>symptoms</strong> usually appear within <strong>about 2-3 weeks after the tick bite</strong> and are often<strong> relatively unspecific</strong>. These include severe <strong>fatigue, fever, loss of appetite, weight loss, pale mucous membranes and jaundice</strong>. A dark red to brown <strong>discoloration of the urine</strong> can also occur, which is caused by the excretion of blood pigments (haemoglobinuria). If left untreated, the disease can lead to consequential damage to various organs, such as <strong>respiratory distress</strong> or <strong>kidney failure</strong>. The <strong>nervous system</strong> can also be affected, which can manifest itself in seizures, paralysis or movement disorders. Without treatment, babesiosis is often fatal. Early diagnosis and treatment are therefore very important.</p><p>As the pathogens are not transmitted directly with the tick bite, but enter the body with a time delay via the tick&#8217;s saliva, rapid removal of the tick and suitable tick protection can reduce the risk of babesiosis. A veterinarian should be contacted immediately in case of suspicion.</p><p>On our website <a href="https://vbd.laboklin.com"><strong>https://vbd.laboklin.com</strong></a> you will find useful information on babesiosis and other <strong>vector-borne</strong> <strong>infectious</strong> diseases (transmitted by mosquitoes or ticks, for example).</p></div>						</div>
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		<title>Primary hyperparathyroidism (PHPT) in the Keeshond</title>
		<link>https://labogen.com/en/2026/03/10/primary-hyperparathyroidism-phpt-in-the-keeshond/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Tue, 10 Mar 2026 10:43:46 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<category><![CDATA[Genetic test]]></category>
		<guid isPermaLink="false">https://labogen.com/2026/03/10/primary-hyperparathyroidism-phpt-in-the-keeshond/</guid>

					<description><![CDATA[Primary hyperparathyroidism (PHPT) in the Keeshond Primary hyperparathyroidism (PHPT) is a hereditary disease in which the regulation of calcium levels in the body is disturbed. Possible consequences are an increasing weakening of the bones, kidney problems and even kidney failure as well as other metabolic disorders. A variant in the SIRT6 gene was found in [&#8230;]]]></description>
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							<h2>Primary hyperparathyroidism (PHPT) in the Keeshond</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>Primary hyperparathyroidism (PHPT) is a hereditary disease in which the regulation of calcium levels in the body is disturbed. Possible consequences are an increasing <strong>weakening of the bones</strong>, <strong>kidney problems</strong> and even kidney failure as well as <strong>other metabolic disorders</strong>.</p><p>A variant in the <em>SIRT6 gene</em> was found in the <strong>Wolfspitz/Keeshond </strong>that is associated with the disease. This is inherited <strong>in an autosomal dominant manner.</strong>  The <strong>late onset of the disease</strong> is particularly challenging for breeders, as the symptoms of PHPT usually only become apparent after the age of 8 and therefore often at a time when the dogs have already been used for breeding. The genetic test enables early identification of affected animals and supports breeders and owners in responsible breeding selection and prevention.</p></div>						</div>
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		<title>Available again: Adult Onset Neuropathy (AON)</title>
		<link>https://labogen.com/en/2026/03/10/available-again-adult-onset-neuropathy-aon/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Tue, 10 Mar 2026 10:26:44 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<category><![CDATA[Genetic test]]></category>
		<guid isPermaLink="false">https://labogen.com/2026/03/10/available-again-adult-onset-neuropathy-aon/</guid>

					<description><![CDATA[Available again: Adult Onset Neuropathy (AON) in the English Cocker Spaniel and Field Spaniel The genetic test for Adult Onset Neuropathy (AON) is now available again! The test is carried out by a partner laboratory and is offered for the English Cocker Spaniel and Field Spaniel breeds. AON is a hereditary disease whose symptoms are [&#8230;]]]></description>
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							<h2>Available again: Adult Onset Neuropathy (AON) in the English Cocker Spaniel and Field Spaniel</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>The genetic test for Adult Onset Neuropathy (AON) is now available again! The test is carried out by a partner laboratory and is offered for the <strong>English Cocker Spaniel and Field Spaniel breeds</strong>.</p><p>AON is a hereditary disease whose symptoms are similar to those of degenerative myelopathy (DM). The first symptoms typically appear at the <strong>age of 7.5 to 9 years</strong> and are characterized by <strong>weakness of the hind legs</strong>, resulting in an uncoordinated gait and a wide-legged stance. As the disease progresses, the <strong>weakness spreads to the front legs</strong> and can eventually lead to <strong>difficulty swallowing</strong>.</p></div>						</div>
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		<title>Clopidogrel efficacy in the cat</title>
		<link>https://labogen.com/en/2026/01/29/clopidogrel-efficacy-in-the-cat/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Thu, 29 Jan 2026 10:41:23 +0000</pubDate>
				<category><![CDATA[Cat]]></category>
		<category><![CDATA[Genetic test]]></category>
		<guid isPermaLink="false">https://labogen.com/2026/01/29/clopidogrel-efficacy-in-the-cat/</guid>

					<description><![CDATA[Clopidogrel efficacy in the cat Arterial thromboembolism (ATE) is a serious and often life-threatening complication in cats with hypertrophic cardiomyopathy (HCM) or other heart diseases. It occurs when a blood clot (thrombus) blocks an artery and thus interrupts the flow of blood to organs or limbs. The consequences are often severe tissue damage or infarctions. [&#8230;]]]></description>
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							<h2>Clopidogrel efficacy in the cat</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p><strong>Arterial thromboembolism (ATE)</strong> is a serious and <strong>often life-threatening</strong> complication in cats with <strong>hypertrophic cardiomyopathy (HCM)</strong> or other <strong>heart diseases</strong>. It occurs when a <strong>blood clot (thrombus)</strong> blocks an artery and thus interrupts the flow of blood to organs or limbs. The consequences are often severe <strong>tissue damage</strong> or<strong> infarctions</strong>.</p><div><strong>Clopidogrel</strong>, an <strong>antiplatelet agent</strong> that inhibits the formation of blood clots by blocking <strong>ADP receptors </strong>, is often used to <strong>prevent ATE</strong> in affected animals. In practice, however, the effectiveness of the therapy varies greatly, which indicates the presence of <strong>clopidogrel resistance</strong> in some animals.</div><div> <br>Scientific studies have now identified a <strong>genetic variant of the <em>P2RY1 gene</em> </strong>that codes for one of the ADP receptors. Cats carrying this variant tend to respond <strong>less well to clopidogrel</strong> and therefore require an <strong>alternative or additional therapy</strong> for thrombosis prophylaxis in order to effectively reduce the risk of ATE.</div></div>						</div>
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		<title>Hypertrophic cardiomyopathy (HCM) in the Golden Retriever</title>
		<link>https://labogen.com/en/2026/01/29/hypertrophic-cardiomyopathy-hcm-in-the-golden-retriever/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Thu, 29 Jan 2026 10:33:50 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<category><![CDATA[Genetic test]]></category>
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					<description><![CDATA[Hypertrophic cardiomyopathy (HCM) in the Golden Retriever Hypertrophic cardiomyopathy (HCM) is a genetic heart disease in which there is an abnormal thickening of the left ventricle. As this ventricle is responsible for the blood supply to the entire body, HCM can significantly impair the heart&#8217;s pumping capacity. This can result in a reduced oxygen supply [&#8230;]]]></description>
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							<h2>Hypertrophic cardiomyopathy (HCM) in the Golden Retriever</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p><strong>Hypertrophic cardiomyopathy (HCM)</strong> is a <strong>genetic heart disease</strong> in which there is an abnormal thickening of the left ventricle. As this ventricle is responsible for the blood supply to the entire body, HCM can <strong>significantly impair</strong> the <strong>heart&#8217;s pumping capacity</strong>. This can result in a reduced oxygen supply to the organs.</p><p>The disease can have serious consequences, including <strong>cardiac arrhythmia, abnormal blood clotting</strong> (risk of thrombosis) and <strong>heart failure</strong>. The clinical symptoms are highly variable and range from <strong>reduced exercise tolerance</strong> and <strong>breathing difficulties</strong> to <strong>fainting or collapse</strong>.<br><br>A <strong>genetic variant in the <em>TNNI3 gene</em></strong> associated with HCM has been identified in a family of Golden Retrievers. The disease is believed to be inherited in an autosomal recessive manner and, in the worst case, can lead to sudden cardiac death.</p></div>						</div>
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		<title>Cerebellar abiotrophy (CA) in the Australian Kelpie</title>
		<link>https://labogen.com/en/2026/01/29/cerebellar-abiotrophy-ca-in-the-australian-kelpie/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Thu, 29 Jan 2026 10:27:50 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<category><![CDATA[Genetic test]]></category>
		<guid isPermaLink="false">https://labogen.com/2026/01/29/cerebellar-abiotrophy-ca-in-the-australian-kelpie/</guid>

					<description><![CDATA[Cerebellar abiotrophy (CA) in the Australian Kelpie Cerebellar abiotrophy (CA) is a hereditary neurological disorder that causes changes in the cerebellum, which is particularly responsible for movement coordination and balance. Two genetic risk markers associated with CA have been identified in the Australian Kelpie. Clinical manifestations of the disease include pronounced ataxia, head tremor, a [&#8230;]]]></description>
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							<h2>Cerebellar abiotrophy (CA) in the Australian Kelpie</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p><strong>Cerebellar abiotrophy (CA) </strong>is a <strong>hereditary neurological disorder</strong> that causes changes in the <strong>cerebellum</strong>, which is particularly responsible for movement coordination and balance.</p><p><strong>Two genetic risk markers</strong> associated with CA have been identified in the <strong>Australian Kelpie</strong>. Clinical manifestations of the disease include <strong>pronounced ataxia</strong>, <strong>head tremor</strong>, a <strong>wide-legged stance of the hind limbs</strong> and a <strong>conspicuous gait pattern</strong> in which the legs are raised excessively when walking.</p><p>One variant affects the LINGO3 gene and is inherited in an autosomal recessive manner with incomplete penetrance. The first symptoms of this variant can appear as early as 4 to 10 weeks of age, although the severity of the symptoms can vary greatly. The second variant in the VPM1 gene shows a later onset of the disease (from about 4-6 months or older) and follows an autosomal recessive inheritance with complete penetrance.<br>Genetic testing makes it possible to identify carrier animals at an early stage and make well-founded breeding decisions.</p></div>						</div>
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		<title>Hypothyroidism in dogs &#8211; new possibilities in diagnostics</title>
		<link>https://labogen.com/en/2025/12/10/hypothyroidism-in-dogs-new-possibilities-in-diagnostics/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Wed, 10 Dec 2025 13:34:38 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<guid isPermaLink="false">https://labogen.com/2025/12/10/hypothyroidism-in-dogs-new-possibilities-in-diagnostics/</guid>

					<description><![CDATA[Hypothyroidism in dogs &#8211; new possibilities in diagnostics Hypothyroidism (underactive thyroid) is one of the most common hormonal diseases in dogs. The thyroid gland produces too few hormones (especially T4), which are important for the entire metabolism. Typical signs are weight gain despite a normal amount of food, tiredness and reduced playfulness, skin and coat [&#8230;]]]></description>
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							<h2>Hypothyroidism in dogs &#8211; new possibilities in diagnostics</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p><strong>Hypothyroidism (underactive thyroid)</strong> is one of the most common <strong>hormonal diseases</strong> in dogs. The <strong>thyroid gland</strong> produces too few hormones (especially T4), which are important for the entire metabolism. Typical signs are <strong>weight gain</strong> despite a normal amount of food, <strong>tiredness</strong> and reduced playfulness<strong>, skin and coat problems</strong>, increased <strong>sensitivity to cold</strong> and sometimes <strong>changes in behavior</strong><strong>.</strong></p><p>As these symptoms can also occur in many other diseases, a measurement of thyroid hormones alone (especially T4 and TSH) is often not sufficient for a reliable diagnosis. A low T4 level in the blood does not automatically mean hypothyroidism &#8211; other non-thyroidal illnesses (NTI) or certain medications can also lower T4. In addition, various interfering factors can distort the measurements.</p><p>In order to gain more clarity in unclear cases &#8211; such as suspected hypothyroidism with low T4 but unchanged TSH &#8211; additional tests are now available at Laboklin. The determination of the <strong>thyroid hormone rT3</strong> (reverse T3) provides additional information as to whether an altered hormone status is more consistent with a genuine hypothyroidism or can be explained by another underlying disease (NTI). In addition, thyroid hormones can be determined using a particularly precise mass spectrometric measurement method known as <strong>LC-MS/MS</strong>. This technique is less susceptible to interference and gives a very reliable picture of the actual hormone concentrations.</p><p>Based on the clinical findings of your veterinarian, these modern analyses help to avoid unnecessary or too late thyroid therapy and thus to find the best possible, individually suitable treatment for your dog.</p><p>If you have any questions, please contact your veterinary practice or veterinary clinic &#8211; they will be happy to help you.</p></div>						</div>
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		<title>Glycogen storage disease (GSD-PGBM1) in the Basset Hound</title>
		<link>https://labogen.com/en/2025/12/10/glycogen-storage-disease-gsd-pgbm1-in-the-basset-hound/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Wed, 10 Dec 2025 13:25:52 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<category><![CDATA[Genetic test]]></category>
		<guid isPermaLink="false">https://labogen.com/2025/12/10/glycogen-storage-disease-gsd-pgbm1-in-the-basset-hound/</guid>

					<description><![CDATA[Glycogen storage disease (GSD-PGBM1) in the Basset Hound Glycogen storage diseases (GSDs) are hereditary metabolic disorders in which too much glycogen is stored in various tissues due to faulty enzymes. A genetic variant in the RBCK1 gene was discovered in the Basset Hound, which leads to the formation of so-called polyglucosan storage bodies and can [&#8230;]]]></description>
										<content:encoded><![CDATA[		<div data-elementor-type="wp-post" data-elementor-id="286479" class="elementor elementor-286479 elementor-285538">
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							<h2>Glycogen storage disease (GSD-PGBM1) in the Basset Hound</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>Glycogen storage diseases (GSDs) are hereditary <strong>metabolic disorders</strong> in which too much glycogen is stored in various tissues due to faulty enzymes. A <strong>genetic variant </strong>in the<strong> <em>RBCK1 gene</em></strong> was discovered in the Basset Hound, which leads to the formation of so-called polyglucosan storage bodies and can cause serious health problems. Affected dogs often initially show <strong>chronic vomiting</strong> and <strong>diarrhea</strong>, usually from around <strong>8 to 12 months of</strong> age. Later on, progressive <strong>muscle weakness</strong>, <strong>exercise intolerance</strong> and serious <strong>heart problems</strong> with heart failure and even sudden cardiac death can occur.</p><p>As the disease progresses gradually and often causes only minimal changes in blood values at the beginning, genetic testing can provide valuable information for the diagnosis. In addition, carrier animals can be identified at an early stage using the genetic test, which is of great importance for responsible breeding planning.</p></div>						</div>
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		<title>Update: Hypertrophic cardiomyopathy (HCM3) in the Ragdoll</title>
		<link>https://labogen.com/en/2025/12/10/update-hypertrophic-cardiomyopathy-hcm3-in-the-ragdoll/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Wed, 10 Dec 2025 13:21:18 +0000</pubDate>
				<category><![CDATA[Cat]]></category>
		<category><![CDATA[Genetic test]]></category>
		<guid isPermaLink="false">https://labogen.com/2025/12/10/update-hypertrophic-cardiomyopathy-hcm3-in-the-ragdoll/</guid>

					<description><![CDATA[Update: Hypertrophic cardiomyopathy (HCM3) in the Ragdoll Hypertrophic cardiomyopathy (HCM) is the most common heart disease in cats. This causes the muscles of the left ventricle to thicken, making it harder for the heart to fill. This can lead to poor performance, shortness of breath, blood clots and, in the worst case, sudden cardiac death. [&#8230;]]]></description>
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							<h2>Update: Hypertrophic cardiomyopathy (HCM3) in the Ragdoll</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>Hypertrophic cardiomyopathy (HCM) is the most common <strong>heart disease</strong> in cats. This causes the muscles of the left ventricle to thicken, making it harder for the heart to fill. This can lead to poor performance, shortness of breath, blood clots and, in the worst case, sudden cardiac death.</p><p>In addition to <strong>ultrasound examinations</strong>, <strong>specific</strong> <strong>genetic tests</strong> are available for some breeds: The <strong>HCM1</strong> variant in the <em>MYBPC3 gene</em> has been described in the <strong>Maine Coon</strong>, the <strong>HCM3</strong> variant in the <em>MYBPC3 gene</em> in the <strong>Ragdoll </strong>and the <strong>HCM4</strong> variant in the <em>ALMS1 gene</em> in the <strong>Sphynx</strong>. These variants are considered <strong>high-risk factors</strong> that can provide an indication of the development of the disease even before the clinical signs appear. Nevertheless, severe, symptomatic forms of the disease usually only develop in combination with other genetic or environmental factors &#8211; a reliable prognosis of the clinical course is therefore not possible on the basis of genetic analyses alone. In addition, these are very <strong>breed-specific variants </strong>for which a correlation with the occurrence of the disease could only be proven in the breeds described in each case.  </p><p>The evaluation of the samples submitted to us between 2012 and 2022 showed a significant decrease in the <strong>HCM3 allele frequency within the Ragdoll breed from 28.6 % to 4.3 %</strong>, which is probably due to breeding efforts. The current distribution of genotypes in the Ragdoll can be seen in the diagram opposite. In addition, we tested around 28,000 cats of various breeds &#8211; in particular British Shorthair, Maine Coon and Persian &#8211; for the Ragdoll variant HCM3. Outside of the Ragdoll breed, it only occurred in negligible numbers, although it is unclear whether there is a correlation with clinical symptoms. We therefore continue to recommend the <strong>HCM3 test</strong> <strong>exclusively for the Ragdoll breed.</strong></p></div>						</div>
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		<title>Ridge in the Rhodesian Ridgeback</title>
		<link>https://labogen.com/en/2025/12/10/ridge-in-the-rhodesian-ridgeback/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Wed, 10 Dec 2025 13:14:16 +0000</pubDate>
				<category><![CDATA[Dog]]></category>
		<category><![CDATA[Genetic test]]></category>
		<guid isPermaLink="false">https://labogen.com/2025/12/10/ridge-in-the-rhodesian-ridgeback/</guid>

					<description><![CDATA[Determination of the ridge gene in the Rhodesian Ridgeback The ridge &#8211; the distinctive ridge running against the direction of the coat &#8211; is one of the characteristic features of the Rhodesian Ridgeback breed. The appearance of the Ridge is clearly defined by the respective breed standards. The development of the ridge is caused by [&#8230;]]]></description>
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							<h2>Determination of the ridge gene in the Rhodesian Ridgeback</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>The <strong>ridge</strong> &#8211; the distinctive <strong>ridge</strong> running against the direction of the coat &#8211; is one of the characteristic features of the Rhodesian Ridgeback breed. The appearance of the Ridge is clearly defined by the respective breed standards.</p><p>The development of the ridge is caused by a <strong>genetic variant on chromosome 18</strong>. This is a <strong>duplication</strong> of an approx. 100 kb long DNA section. The variant follows an <strong>autosomal dominant inheritance with incomplete penetrance</strong>: in heterozygous dogs with the R/r genotype, around 95% carry a ridge, while in around 5% of dogs the dominant R allele is silenced, meaning that these dogs do not have a ridge.</p><p>The genetic test can be used to determine whether the ridge gene is heterozygous (R/r) or homozygous (R/R). The genotypes of the mating partners can be used to predict whether puppies without a ridge can be expected in the offspring.</p><p>Our tip: We also offer a new practical Ridge + Dermoidsinus (DS) combination package!  </p></div>						</div>
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