Deficiency In Pigs Research Articles

Reconstruction of medial meniscus posterior portion deficiency in pigs with an autologous patellar tendon graft: an experimental study

ObjectiveThis study was performed to investigate the effectiveness of two surgical procedures, autologous patellar tendon graft reconstruction and trans-tibial plateau pull-out repair, using a pig model. The primary focus was to assess the repair capability of medial meniscus posterior portion (MMPP) deficiency, the overall structural integrity of the meniscus, and protection of the femoral and tibial cartilage between the two surgical groups. The overall aim was to provide experimental guidelines for clinical research using these findings.MethodsTwelve pigs were selected to establish a model of injury to the MMPP 10 mm from the insertion point of the tibial plateau. They were randomly divided into three groups of four animals each: reconstruction (autologous tendon graft reconstruction of the MMPP), pull-out repair (suture repair of the MMPP via a trans-tibial plateau bone tunnel), and control (use of a normal medial meniscus as the negative control). The animals were euthanized 12 weeks postoperatively for evaluation of the meniscus, assessment of tendon bone healing, and gross observation of knee joint cartilage. The tibial and femoral cartilage injuries were evaluated using the International Society for Cartilage Repair (ICRS) grade and Mankin score. Histological and immunohistochemical staining was conducted on the meniscus–tendon junction area, primary meniscus, and tendons. The Ishida score was used to evaluate the regenerated meniscus in the reconstruction group. Magnetic resonance imaging (MRI) was used to evaluate meniscal healing.ResultsAll 12 pigs recovered well after surgery; all incisions healed without infection, and no obvious complications occurred. Gross observation revealed superior results in the reconstruction and pull-out repair groups compared with the control group. In the tibial cartilage, the reconstruction group had ICRS grade I injury whereas the pull-out repair and control groups had ICRS grade II and III injury, respectively. The Mankin score was significantly different between the reconstruction and control groups; histological staining showed that the structure of the regenerated meniscus in the reconstruction group was similar to that of the original meniscus. Immunohistochemical staining showed that the degree of type I and II collagen staining was similar between the regenerated meniscus and the original meniscus in the reconstruction group. The Ishida score was not significantly different between the regenerated meniscus and the normal primary meniscus in the reconstruction group. MRI showed that the MMPP in the reconstruction and pull-out repair groups had fully healed, whereas that in the control group had not healed.ConclusionAutologous patellar tendon graft reconstruction of the MMPP can generate a fibrocartilage-like regenerative meniscus. Both reconstruction and pull-out repair can preserve the structural integrity of the meniscus, promote healing of the MMPP, delay meniscal degeneration, and protect the knee cartilage.

Novel edible toys as iron carrier to prevent iron deficiency of postweaned pigs

The current preventive treatment for iron deficiency in pigs is inefficient, resulting in a high prevalence of iron-deficient or anemic postweaned pigs. The aim of this study was to develop and characterize edible toys (ETs) to be used as oral iron supplements, and to assess their effect on feeding behavior and iron status of postweaned pigs. Three types of ETs, varying in sweetness, were produced by ionic gelation, using whey, sodium alginate, ferrous sulfate and atomized bovine erythrocytes. ET control (ETC) was developed without sweetener, ET1 contained 15% w/v sucrose and ET2 contained 0.03% w/v of Sucram (98% sodium saccharin, 1% neosperidine dihydrocalcone and 1% maltol). ETs were mainly composed of carbohydrates and protein, with a similar concentration of iron (2.2–2.7 mg/g). The ETs were offered to 24 postweaned pigs to measure acceptability and preference. The animals preferred ETC and ET2 over ET1. To assess the nutritional benefit of the ETs, 24 postweaned pigs were distributed into three groups: ETC (without iron), ETC-Fe (ETC with iron) and ET2-Fe (with iron and Sucram). Iron-loaded ET (ETC-Fe and ET2-Fe) significantly increased the concentration of red blood cells (from 6.1 to 7.5·106 x mm3 for ETC-Fe and from 6.2 to 7.8 for ET2-Fe), hematocrit (from 32.8 to 37.9% for ETC-Fe and from 32.3 to 35.1 for ET2-Fe), serum iron (from 28.6 to 120.6 µmol/L for ETC-Fe and from 34.9 to 145.4 for ET2-Fe) and serum ferritin (from 7.8 to 18.5 µg/L for ETC-Fe and from 8.1 to 20.2 for ET2-Fe). In conclusion, the ETs developed in this study were accepted by the pigs and provided adequate iron to improve the iron status of postweaned pigs.

Se deficiency induces renal pathological changes by regulating selenoprotein expression, disrupting redox balance, and activating inflammation.

Selenium (Se) is closely associated with kidney disease, and renal injury often occurs together with hyposelenemia. This study was designed to reveal the mechanism underlying renal injury induced by Se deficiency in pigs. Twenty-four castrated male Yorkshire pigs were divided into two groups fed either a Se-deficient diet (0.007 mg Se per kg) or a Se-adequate diet (0.3 mg Se per kg). Serum and kidney samples were collected at the 16th week of the trial, processed, and analyzed for serum biochemistry, Se concentration, kidney index markers, histology, selenoprotein mRNA expression, redox status, and inflammatory cytokines. Dietary Se deficiency induced kidney injury, decreased (P < 0.05) Se concentrations, and increased (P < 0.05) kidney index and serum blood urea nitrogen, creatinine, and carbon dioxide values. Histological analysis indicated that Se deficiency induced inflammatory lesions and renal tubular atrophy in the renal medulla. Se deficiency downregulated (P < 0.05) nine selenoprotein genes (GPX1, SELENOW, SELENOH, SELENOP, GPX3, TXNRD2, SELENOI, SELENON, and SELENOM) and upregulated (P < 0.05) SEPHS2 in the kidneys. Se deficiency decreased (P < 0.05) the activity of glutathione peroxidase, thioredoxin reductase, and catalase, as well as the hydroxyl radical inhibition capacity, and increased (P < 0.05) the content of malondialdehyde and nitric oxide. Se deficiency increased (P < 0.05) the expression of the transcription factors NF-κB and HIF-1α, and regulated inflammatory cytokines. Se deficiency increased (P < 0.05) the expression of IL-6, IL-8, IL-12, IL-17, and cyclooxygenase-2, and decreased (P < 0.05) the expression of IL-10, IL-13, and TGF-β. These results indicated that Se deficiency induces kidney injury through the regulation of selenoproteins, oxidative stress, and inflammation.

MC4R deficiency in pigs results in hyperphagia and ultimately hepatic steatosis without high-fat diet

Melanocortin 4 receptor (MC4R)-deficient mice had been used for several years to study human nonalcoholic steatohepatitis (NASH). However, although liver pathologic and biochemical indicators have been examined, mice models do not always faithfully display the phenotype of the human disease. In this study, we investigated the MC4R knockout phenotype in miniature pigs. We found that pigs lacking MC4R exhibited hyperorexia, insulin resistance, hyperinsulinemia, disordered lipid metabolism and their livers accumulated significant amounts of fat. We have shown that deletion of MC4R results in hyperphagia and increased body fat, ultimately leading to hepatic steatosis without atherogenic diet.

Causation of human ulcerative colitis: A lead from an animal model that mirrors human disease.

Most models of experimental colitis do not replicate human ulcerative colitis and do not help in defining the causation of human ulcerative colitis. Inducing pantothenic acid deficiency in pigs produces an ideal model in terms of extent, histology, and chronicity of human ulcerative colitis. Comparing metabolic changes in human ulcerative colitis with metabolic changes in experimental colitis in pigs provided a guide for the search of initiating factors of human ulcerative colitis. Observations showed that bacterial nitric oxide with bacterial hydrogen sulphide reproduced the metabolic changes of human ulcerative colitis. Decreasing colon‐produced nitric oxide and hydrogen sulphide by bacteria through diet and medication resulted in pronounced therapeutic improvement, both clinically and histologically, of human ulcerative colitis.

Differential Effect of the Deletion of African Swine Fever Virus Virulence-Associated Genes in the Induction of Attenuation of the Highly Virulent Georgia Strain.

African swine fever virus (ASFV) is the etiological agent of an often lethal disease of domestic pigs, African swine fever (ASF). The ASFV Georgia 2007 isolate (ASFV-G) is responsible for the current epidemic situation in Europe and Asia. Genetically modified ASFVs containing deletions of virulence-associated genes have produced attenuated phenotypes and induced protective immunity in swine. Here we describe the differential behavior of two viral genes, NL (DP71L) and UK (DP96R), both originally described as being involved in virus virulence. Deletion of either of these genes efficiently attenuated ASFV strain E70. We demonstrated that deletion of the UK gene from the ASFV-G genome did not decrease virulence when compared to the parental virus. Conversely, deletion of the NL gene produced a heterogeneous response, with early death in one of the animals and transient fever in the other animals. With this knowledge, we attempted to increase the safety profile of the previously reported experimental vaccine ASFV-GΔ9GL/ΔUK by deleting the NL gene. A triple gene-deletion virus was produced, ASFV-GΔ9GL/ΔNL/ΔUK. Although ASFV-GΔ9GL/ΔNL/ΔUK replicated in primary cell cultures of swine macrophages, it demonstrated a severe replication deficiency in pigs, failing to induce protection against challenge with parental ASFV-G.

High mobility group A2 (HMGA2) deficiency in pigs leads to dwarfism, abnormal fetal resource allocation, and cryptorchidism

Expression of HMGA2 is strongly associated with body size and growth in mice and humans. In mice, inactivation of one or both alleles of Hmga2 results in body-size reductions of 20% and 60%, respectively. In humans, microdeletions involving the HMGA2 locus result in short stature, suggesting the function of the HMGA2 protein is conserved among mammals. To test this hypothesis, we generated HMGA2-deficient pigs via gene editing and somatic cell nuclear transfer (SCNT). Examination of growth parameters revealed that HMGA2-/+ male and female pigs were on average 20% lighter and smaller than HMGA2+/+ matched controls (P < 0.05). HMGA2-/- boars showed significant size reduction ranging from 35 to 85% of controls depending on age (P < 0.05), and organ weights were also affected (P < 0.05). HMGA2-/+ gilts and boars exhibited normal reproductive development and fertility, while HMGA2-/- boars were sterile due to undescended testes (cryptorchidism). Crossbreeding HMGA2-/+ boars and gilts produced litters lacking the HMGA2-/- genotype. However, analysis of day (D) D40 and D78 pregnancies indicated that HMGA2-/- fetuses were present at the expected Mendelian ratio, but placental abnormalities were seen in the D78 HMGA2-/- concepti. Additionally, HMGA2-/- embryos generated by gene editing and SCNT produced multiple pregnancies and viable offspring, indicating that lack of HMGA2 is not lethal per se. Overall, our results show that the effect of HMGA2 with respect to growth regulation is highly conserved among mammals and opens up the possibility of regulating body and organ size in a variety of mammalian species including food and companion animals.

The impact of antiandrogen flutamide on the hypoxia inducible factor 1a and vascular endothelial growth factor A gene and protein expression in the pig placenta during late pregnancy.

In contrast to estradiol action, little is known about androgen signaling in placental development. The purpose of this study was to evaluate the impact of diminished androgen action on hypoxia inducible factor 1a (HIF-1a) and vascular endothelial growth factor A (VEGFA) protein expression as well as their mRNAs in the structures of fetal and maternal parts of porcine placenta during late pregnancy. Pregnant pigs were injected daily with antiandrogen flutamide, at a dose of 50 mg/kg body weight at different stages of pregnancy: between gestational days 83-89 (90 dpc) and 101-107 (108 dpc). Control groups (90 dpc or 108 dpc) were treated with vehicle (corn oil). One day after the last injection animals were sacrificed and tissues were collected. Tissue samples were frozen for mRNA isolation or fixed for immu-nohistochemistry (IHC). The expression of HIF-1a and VEGFA were investigated by real-time PCR and IHC. Flutamide treatment caused changes in both HIF-1a and VEGFA mRNA levels only in the placentas of the 90 dpc group. Relative optical density analysis showed decreased HIF-1a and increased VEGFA protein expression in the placentas obtained from flutamide-treated 108 dpc group while no differences were observed in the 90 dpc group. Experimentally induced androgen deficiency in pigs deregulates the expression of some genes important for placental blood circulation. We suggest that androgens are involved in the control of expression of HIF-1a and VEGFA in porcine placenta during late pregnancy.

Degenerative axonopathy associated with copper deficiency in pigs

ABSTRACT: The epidemiological, clinic and morphological (pathological and ultrastructural) aspects of four outbreaks of copper deficiency affecting 21- to 90-day-old pigs in the Northeast region of Brazil are reported. Clinical signs began with paraparesis and ataxia and progressed to flaccid or spastic paralysis of the pelvic and thoracic limbs, followed by sternal and/or lateral recumbence. In addition, some animals showed dog-sitting position and intention tremors. The clinical manifestation period was 5-20 days. Significant gross lesions were not observed; however, microscopically, symmetrical degeneration of the white matter with ballooned myelin sheaths containing occasional macrophages was observed, mainly in the spinal cord. Two pigs presented with necrosis ad loss of Purkinje cells and ectopic Purkinje cells in the granular layer and cerebellar white matter. A ultrastructural analysis showed different degrees of damage of myelinated axons in the spinal segments, including an absence of the axoplasm structures with only axonal residues remaining. The myelin sheaths were degenerated and often collapsed into the space previously occupied by the axon. These results suggest that myelin degeneration is secondary to the axonal lesion. Finally, the concentration of copper in the liver was determined using atomic absorption spectrophotometry and was found to be low (ranging from 2.2 to 10.8 ppm). In conclusion, in the Brazilian semiarid region, Cu deficiency occurs in 21 to 90-day-old pigs that ingested different types of waste in their food.

Iodine deficiency in pigs and the solutions to the problem

The articles provides an overview of literature dedicated to the study of iodine status in pigs and establishes an interrelation between the level of microelement in animal diet and the functional activity of thyroid gland. Close correlation between thyroid hormone levels in blood and the reproductive abilities and productiveness of pigs has been observed. Resulting thyroxin and triiodothyronine synthesis and metabolic disorders are among the most common causes of pathological states in animals, which are characterized by lower fertility, increased intrauterine fetal deaths, and birth of non-viable piglets with apparent signs of goiter. Moreover, thyroid hypofunction leads to decreased general and lipoid metabolism in pigs, young animals in particular. Feed is the source of iodine for pigs. Yet, due to intensive growing practices the primary place in pig nutrition is occupied by concentrated feed with as a rule low content of this microelement. In addition, a number of other factors affect iodine levels in organism. Iodine digestibility is particularly hindered by glucosinolates and cyanogenic glycosides, nitrates, nitrites, perchlorates, residue of some pesticides. Iodine absorption in gastrointestinal tract is slowed down by fluorine and sulfur. Pigs may receive enough iodine with additional feed containing inorganic (КІ, NaІ) and organic (iodates) compounds. For this purpose industrial farms tend to use premixtures and mineral additives containing iodine and other macro- and microelements. However, said forms of iodine-containing preparations are often unstable or even aggressive in combination with other components of additives, namely vitamins. In this connection, we are facing a relevant problem of finding new preparations that in small doses would be stable and compatible with other components of compound feed while solving the problem of microelement nutrition. In humane and veterinary medicine nanomaterials, namely metal aquachelates, are used increasingly more often. There is information as to positive impact that iodine aquacitrate has on animals which needs to be further confirmed by profound research.

Alpha 1,3‐Galactosyltransferase Deficiency in Pigs Increases Sialyltransferase Activities That Potentially Raise Non‐Gal Xenoantigenicity

We examined whether deficiency of the GGTA1 gene in pigs altered the expression of several glycosyltransferase genes. Real-time RT-PCR and glycosyltransferase activity showed that 2 sialyltransferases [α2,3-sialyltransferase (α2,3ST) and α2,6-sialyltransferase (α2,6ST)] in the heterozygote GalT KO liver have higher expression levels and activities compared to controls. Enzyme-linked lectin assays indicated that there were also more sialic acid-containing glycoconjugate epitopes in GalT KO livers than in controls. The elevated level of sialic-acid-containing glycoconjugate epitopes was due to the low level of α-Gal in heterozygote GalT KO livers. Furthermore, proteomics analysis showed that heterozygote GalT KO pigs had a higher expression of NAD+-isocitrate dehydrogenase (IDH), which is related to the CMP-N-acetylneuraminic acid hydroxylase (CMAH) enzyme reaction. These findings suggest the deficiency of GGTA1 gene in pigs results in increased production of N-glycolylneuraminic acid (Neu5Gc) due to an increase of α2,6-sialyltransferase and a CMAH cofactor, NAD+-IDH. This indicates that Neu5Gc may be a critical xenoantigen. The deletion of the CMAH gene in the GalT KO background is expected to further prolong xenograft survival.

Iron Transporters Are Differentially Regulated by Dietary Iron, and Modifications Are Associated with Changes in Manganese Metabolism in Young Pigs1–3

To investigate the effects of dietary iron (Fe) on manganese (Mn) metabolism, 24 weaned pigs (21 d old) were blocked by litter and weight and randomly assigned to the following treatments: 1) no supplemental Fe [low Fe (L-Fe)]; 2) 100 mg supplemental Fe/kg [adequate Fe (A-Fe)]; and 3) 500 mg supplemental Fe/kg [high Fe (H-Fe)]. The basal diet was analyzed to contain 20 mg Fe/kg. Tissues were harvested after 32 d of feeding. Daily gain (least square means ± SEM) was greater in A-Fe pigs (328.3 ± 29.9 g/d) than in L-Fe pigs (224.0 ± 11.2 g/d). Hemoglobin concentrations on d 32 were lower in L-Fe pigs (62 ± 3.5 g/L) than in A-Fe pigs (128 ± 5.6 g/L) and did not differ between pigs fed A-Fe and H-Fe (133 ± 12.0 g/L). Liver Fe increased with increasing dietary Fe. Relative hepatic hepcidin expression was greater in pigs fed A-Fe and H-Fe than in those fed L-Fe. Relative expressions of duodenal divalent metal transporter 1 (DMT1) and solute carrier family 39 member 14 (ZIP14) were increased in L-Fe pigs compared with H-Fe pigs. Liver copper (Cu) was higher in L-Fe (0.56 ± 0.04 mmol/kg) and H-Fe (0.58 ± 0.04 mmol/kg) pigs than in A-Fe pigs (0.40 ± 0.04 mmol/kg). Liver Mn was lower in H-Fe pigs (0.15 ± 0.01 mmol/kg) than in A-Fe (0.23 ± 0.02 mmol/kg) or L-Fe pigs (0.20 ± 0.02 mmol/kg). Duodenal Mn concentrations were greater in L-Fe pigs than in A-Fe or H-Fe pigs. Fe deficiency in pigs increased gene expression of duodenal metal transporters (DMT1 and ZIP14) and supplementation with H-Fe reduced expression of DMT1 and ZIP14, which may have decreased absorption of Mn.

COPPER deficiency in pigs.

Copper Deficiency in Pigs Nutrition Reviews, Volume 9, Issue 10, October 1951, Pages 317–318, https://doi.org/10.1111/j.1753-4887.1951.tb02515.x Published: 01 October 1951

Mineral profiling of local pig-feeds and pigs reared under resource driven production system to reduce porcine mineral deficiency in subtropical hill ecosystem of Northeastern India

The present study assessed the mineral status of pigs fed with local feed resources. The commonly used plants for feeding pigs and blood serum samples from Hampshire, Large White Yorkshire and indigenous pigs were analyzed for total protein, albumin and cholesterol levels. Processed plant and serum samples were also analyzed for calcium, phosphorus, magnesium, sodium, potassium, copper, cobalt, manganese, iron and zinc. The incidence and extent of mineral deficiency in pigs was quantified. No significant difference was observed in total protein and albumin levels between any two breed/types of pigs, however the Indigenous pigs showed significantly (P < 0.05) higher cholesterol level compared to other two breeds. Among different plants, Spilanthus sp had majority of macro and micro nutrients in high levels. Regarding incidence of mineral deficiency in pigs, it was observed that 90, 67.1, 61.4, 48.6, 95.7% of the pigs were deficient in calcium, phosphorus, sodium, magnesium and potassium. An interesting finding was that all the pigs (100%) utilized in the study were deficient in zinc. From this study, it was inferred that there are good numbers of potential source of mineral that might be used more economically to improve the mineral availability to pigs.

Intragenic deletion in the gene encoding L-gulonolactone oxidase causes vitamin C deficiency in pigs.

The absence of L-ascorbic acid (L-AA, or AA) synthesis in scurvy-prone organisms, including humans, other primates, guinea pigs, and flying mammals, was traced to the lack of L-gulonolactone oxidase (GULO) activity. GULO is a microsomal enzyme that catalyzes the terminal step in the biosynthesis of L-AA. Clinical cases of scurvy were described in a family of Danish pigs. This trait is controlled by a single autosomal recessive allele designated od (osteogenic disorder). Here we demonstrate that the absence of GULO activity and the associated vitamin C deficiency in od/od pigs is due to the occurrence of a 4.2-kbp deletion in the GULO gene. This deletion includes 77 bp of exon VIII, 398 bp of intron 7 and 3.7 kbp of intron 8, which leads to a frame shift. The mutant protein is truncated to 356 amino acids, but only the first 236 amino acids are identical to the wild-type GULO protein. In addition, the od allele seems to be less expressed in deficient and heterozygous pigs compared with the normal allele in heterozygous and wild-type animals as determined by ribonuclease protection assay. We also developed a DNA-based test for the diagnosis of the deficient allele. However, we failed to identify the mutated allele in other pig populations.

Marginal vitamin A deficiency in pigs experimentally infected with Trichuris suis: a model for vitamin A inadequacy in children

The development of an experimental model for marginal vitamin A deficiency in humans is of major interest, enabling the elucidation of possible interactions with helminth infections. We established a useful experimental model for human vitamin A deficiency in young pigs; deficiency was induced through a depletion method encompassing both sow and offspring. We report on a 2 × 2 study in which 18-week-old vitamin A deficient pigs and vitamin A sufficient littermates were infected with both of the intestinal nematodes Trichuris suis and Ascaris suum and followed for 14 weeks through 32 weeks of age. Forty-nine pigs were followed with respect to bodyweight, liver biopsies and blood samples for retinol concentration and faecal samples for parasite eggs and worms. Liver and serum concentrations of vitamin A were significantly diminished in the vitamin A deficient (VAD) group as compared to the vitamin A sufficient (VAS) group both before ( P < 0·001) and after inoculation with T. suis and A. suum ( P < 0·02). A significant correlation between retinol content in micro-biopsy needle samples and gross liver content was found ( r = 0·457, n = 48, P = 0·001). The adult T. suis worms in the VAD group were marginally smaller (36·7 vs 40·2 mm; P = 0·08), more orally located (section 2·9 vs 3·9; P = 0·08) and had a higher proportion of males (0·58 vs 0·50; P = 0·08) whereas there were no effects of diet treatment on fecundity. The proportion of pigs with faecal T. suis egg excretion 12 weeks post inoculation (p.i.) was significantly lower in the VAD group compared with the VAS infected group (21 vs 78%; P = 0·036). In addition, faecal T. suis egg excretion was significantly lower in the VAD group at both week 11 ( P = 0·040) and week 12 p.i. ( P = 0·021). Vitamin A deficiency may have altered the functional integrity of the mucosal intestinal epithelium, disrupting the normally delicate attachment of T. suis and leading to the premature termination of infection. However, a possible antagonistic interaction, if verified, should not preclude interventions to improve vitamin A status, i.e., treatment should accompany anthelmintic treatment.

The L-gulono-gamma-lactone oxidase gene (GULO) which is a candidate for vitamin C deficiency in pigs maps to chromosome 14.

Vitamin C deficient pigs, when fed a diet lacking L-ascorbic acid (AscA), manifest deformity of the legs, multiple fractures, osteoporosis, growth retardation and haemorrhagic tendencies. This trait was shown by others to be controlled by a single autosomal recessive allele designated as od (osteogenic disorder). The inability of AscA biosynthesis in primates and guinea pigs that exhibit similar symptoms, when they are not supplemented with AscA in the food, was traced to the lack of L-gulono-gamma-lactone oxidase, which catalyzes the terminal step in the biosynthesis of AscA. The non-functional GULOP was mapped to human chromosome 8p21 that corresponds to an evolutionarily conserved segment on either porcine chromosome 4 (SSC4) or 14 (SSC14). We investigated linkage between OD and SSC4- and 14-specific microsatellite loci in order to map the OD locus. Twenty-seven informative meioses in families from one sire and three dams revealed linkage of od with microsatellites SW857 and S0089, located in the subcentromeric region of SSC14. We isolated part of the GULO gene of the pig by screening a porcine genomic library using a pig GULO cDNA as a probe, and mapped it to SSC14q14 by fluorescence in situ hybridization (FISH). Thus, the porcine GULO gene is both a good physiological and positional candidate gene for vitamin C deficiency in pigs.

Genetic studies into inherited and sporadic hemolytic uremic syndrome

Genetic studies into inherited and sporadic hemolytic uremic syndrome

Genetic studies into inherited and sporadic hemolytic uremic syndrome

Hemolytic uremic syndrome (HUS) in adults carries a high morbidity and mortality, and its cause remains unknown despite many theories. Although familial HUS is rare, it affords a unique opportunity to elucidate underlying mechanisms that may have relevance to acquired HUS. We have undertaken a genetic linkage study based on a candidate gene approach. A common area bounded by the markers D1S212 and D1S306, a distance of 26 cM located at 1q32 segregated with the disease (Z max 3.94). We demonstrate that the gene for factor H lies within the region. Subsequent mutation analysis of the factor H gene has revealed two mutations in patients with HUS. In an individual with the sporadic/relapsing form of the disease we have found a mutation comprising a deletion, subsequent frame shift and premature stop codon leading to half normal levels of serum factor H. In one of the three families there is a point mutation in exon 20 causing an arginine to glycine change, which is likely to alter structure and hence function of the factor H protein. Factor H is a major plasma protein that plays a critical regulatory role in the alternative pathway of complement activation. In light of these findings and previous reports of HUS in patients with factor H deficiency, we postulate that abnormalities of factor H may be involved in the etiology of HUS.

Effects of dietary tryptophan deficiency in finishing pigs, according to age or weight at slaughter or live weight gain

Abstract Three experiments were conducted with 188 finishing pigs (females and castrated males) of the Large White breed, between mean body weights (BW) of 53 and 88 kg, and fed according to a feeding scale, to study the effects of dietary tryptophan (TRP) deficiency (0.10 vs. 0.13%) on feed intake, growth performance, body composition and tissue gain, and meat quality, according to age or BW at slaughter or BW gain. TRP deficiency depressed feed intake, growth performance, and tissue (muscle and fat) gains, with less pronounced effect with advancing age. Females were more sensitive to TRP deficiency than castrated males. The weights of lean and fat joints both decreased with TRP deficiency in pigs slaughtered at the same age, with no resulting change in carcass composition, while they were similar to those in control animals after slaughter at the same BW. The addition of dietary limiting TRP affected carcass conformation through preferential stimulation of development in depth (forehand, hindquarter) compared to development in length, thus producing longer carcasses at the same age at slaughter, but shorter carcasses when pigs were slaughtered at the same BW. This was also the case after feed restriction, for similar gain as in TRP-deficient animals. There was no effect of dietary TRP on muscle quality characteristics. The results were discussed in relation to the common stimulating effect of the limiting dietary factor for growth, whether amino acid or energy, on the development of the early maturing body compartments and the resulting changes in carcass conformation according to age or weight at slaughter.