Effect of the ratio between essential and nonessential amino acids in the diet on utilization of nitrogen and amino acids by growing pigs.

In 36 growing pigs (30 to 60 kg), N balance and amino acid (AA) composition of weight gain were measured to evaluate the interactive effect of the ratio between N from essential amino acids (EAA(N)) to nonessential amino acids (NEAA(N)) and total N level (T(N)) in the diet on N retention and utilization of N, EAA(N), NEAA(N), and AA. Nine diets composed from ordinary feedstuffs and supplemented with crystalline AA were used (three EAA(N):NEAA(N) ratios of 38:62, 50:50, and 62:38 at three T(N) levels of 18.8, 22.9, and 30.0 g/kg). Pigs were fed restrictedly, at a level of 2.8 x energy for maintenance. In all diets, EAA (including arginine) supply was according to or slightly above the recommended ratios to lysine. Measurements were done in four blocks of nine pigs each. In a concomitant slaughter experiment, the AA composition of deposited body protein was determined to estimate AA utilization. The effects of T(N) and EAA(N):NEAA(N) and their interaction for N retention and utilization were significant. Nitrogen retention increased with higher T(N) in the diet. Increasing EAA(N):NEAA(N) from 38:62 to 50:50 improved N retention only at the two lower T(N) levels. Increasing EAA(N): NEAA(N) above 50:50 failed to improve N retention significantly at any of the three T(N) levels. Lowering T(N) improved the utilization of total and digested N and of EAA(N) and NEAA(N). The increase in EAA(N): NEAA(N) consistently resulted in a lower utilization of EAA(N), but this was compensated by a higher utilization of NEAA(N). The utilization of T(N) was improved by increasing EAA(N):NEAA(N) from 38:62 to 50:50 at the two lower T(N) levels and was relatively unaffected by EAA(N):NEAA(N) at the highest T(N). However, a lower utilization of N was observed at a ratio of 62:38 at a T(N) level of 22.9 g/kg. The effects were similar for utilization of individual EAA and NEAA. Utilization of alanine, aspartic acid, and glycine was close to or >100% at the highest EAA(N):NEAA(N), which was expected because all of these AA are synthesized in pigs. Also, the utilization of arginine was >100% in most of the treatments, which confirms the semiessential character of this AA for maintenance. We concluded that the required ratio of EAA(N):NEAA(N) for optimal N retention and utilization is approximately 50:50. The EAA(N):NEAA(N) is more important at lower dietary protein levels. This study indicates that EAA(N): NEAA(N) can be increased up to 70:30 without lowering the utilization of N. Thus, deaminated EAA(N) was efficiently utilized for the synthesis of NEAA(N).     

Effect of furosemide on performance of Thoroughbreds racing in the United States and Canada.

OBJECTIVE: To determine the effect of furosemide on performance of Thoroughbreds racing on dirt surfaces at tracks in the United States and Canada. DESIGN: Cross-sectional study. ANIMALS: All Thoroughbreds (n = 22,589) that finished a race on dirt surfaces at tracks in the United States and Canada between June 28 and July 13, 1997 in jurisdictions that allowed the use of furosemide. PROCEDURE: Race records were analyzed by use of multivariable ANOVA procedures and logistic regression analyses to determine the effect of furosemide on estimated 6-furlong race time, estimated racing speed, race earnings, and finish position. Principal component analysis was used to create orthogonal scores from multiple collinear variables for inclusion in the models. RESULTS: Furosemide was administered to 16,761 (74.2%) horses. Horses that received furosemide raced faster, earned more money, and were more likely to win or finish in the top 3 positions than horses that did not. The magnitude of the effect of furosemide on estimated 6-furlong race time varied with sex, with the greatest effect in males. When comparing horses of the same sex, horses receiving furosemide had an estimated 6-furlong race time that ranged from 0.56 +/- 0.04 seconds (least-squares mean +/- SE) to 1.09 +/- 0.07 seconds less than that for horses not receiving furosemide, a difference equivalent to 3 to 5.5 lengths. CONCLUSIONS AND CLINICAL RELEVANCE: Because of the pervasive use of furosemide and its apparent association with superior performance in Thoroughbred racehorses, further consideration of the use of furosemide and investigation of its effects in horses is warranted.     

Cardiovascular effects of medetomidine, detomidine and xylazine in horses

The cardiovascular effects of medetomidine, detomidine, and xylazine in horses were studied. Fifteen horses, whose right carotid arteries had previously been surgically raised to a subcutaneous position during general anesthesia were used. Five horses each were given the following 8 treatments: an intravenous injection of 4 doses of medetomidine (3, 5, 7.5, and 10 microg/kg), 3 doses of detomidine (10, 20, and 40 microg/kg), and one dose of xylazine (1 mg/kg). Heart rate decreased, but not statistically significant. Atrio-ventricular block was observed following all treatments and prolonged with detomidine. Cardiac index (CI) and stroke volume (SV) were decreased with all treatments. The CI decreased to about 50% of baseline values for 5 min after 7.5 and 10 microg/kg medetomidine and 1 mg/kg xylazine, for 20 min after 20 microg/kg detomidine, and for 50 min after 40 microg/kg detomidine. All treatments produced an initial hypertension within 2 min of drug administration followed by a significant decrease in arterial blood pressure (ABP) in horses administered 3 to 7.5 microg/kg medetomidine and 1 mg/kg xylazine. Hypertension was significantly prolonged in 20 and 40 microg/kg detomidine. The hypotensive phase was not observed in 10 microg/kg medetomidine or detomidine. The changes in ABP were associated with an increase in peripheral vascular resistance. Respiratory rate was decreased for 40 to 120 min in 5, 7.5, and 10 microg/kg medetomidine and detomidine. The partial pressure of arterial oxygen decreased significantly in 10 microg/kg medetomidine and detomidine, while the partial pressure of arterial carbon dioxide did not change significantly. Medetomidine induced dose-dependent cardiovascular depression similar to detomidine. The cardiovascular effects of medetomidine and xylazine were not as prolonged as that of detomidine. KEY WORDS: cardiovascular effect, detomidine, equine, medetomidine, xylazine.     

Effects of dietary carbohydrates and buffering capacity on nutrient digestibility and manure characteristics in finishing pigs

A 2 x 3 factorial experiment was conducted with 24 finishing pigs (Yorkshire x [Finnish Landrace x Dutch Landrace]) to determine the effects of dietary buffering capacity (BC) and carbohydrate sources on apparent total tract digestibility (TD), N retention, and manure characteristics. Twelve of these pigs were fitted with steered ileo-cecal value cannulas to measure the apparent ileal digestibility (ID) of N. Experimental variables were two levels of BC (High = 600 mEq/kg and Low = 530 mEq/kg) and three dietary carbohydrates (tapioca [28%], soybean hulls [25%], and sugar beet pulp [25%]). The two levels of BC were achieved by adjusting the amounts of alkalogenic limestone and acidogenic Ca sulfate in the diet. Pigs were fed twice daily at 2.4 x maintenance requirement for metabolizable energy (418 kJ ME/BW(0.75)). Chromic oxide was used as an indigestible marker. Feces and urine were collected over 5 d for nutrient balance and in vitro measurements of pH and ammonia emission over 7 d. No significant interactions between BC and dietary carbohydrates on the ID, TD, N retention, or manure characteristics were observed. Lowering BC with Ca sulfate did not affect digestibility of most nutrients, except for a negative impact on the TD of Ca (P = 0.015) and Mg (P = 0.003). Although all pigs receiving Ca sulfate had more acidic urine (by 0.49 pH units; P = 0.001), ammonia emission from manure was not lowered, irrespective of the carbohydrate source. Carbohydrates affected significantly the ID and TD of most nutrients, whereas N retention remained similar (P > 0.10). Urinary N:fecal N ratios in manure of pigs fed diets with tapioca, soybean hulls, and beet pulp were 2.09, 1.35, and 1.67, respectively. These ratios corresponded with in vitro ammonia emission (169, 125, and 148 mmol/7 d; P = 0.023). In conclusion, these results indicate that the acidification of urine in pigs fed Ca sulfate in the presence of NSP-rich carbohydrates was achieved. However, acidity of manure and ammonia emission were not affected. The addition of NSP from soybean hulls and(or) sugar beet pulp reduced ratios of urinary:fecal N, and thereby ammonia emission.     

沙对高尔夫果岭坪床物理特性的影响

对28种沙与泥炭按75∶25混配而成的高尔夫果岭坪床材料的物理特性进行了评价。不同类型沙的粒径、均一性和形状有所不同。高尔夫果岭坪床的物理特性主要取决于所使用的沙的特性。对沙 泥炭混配的坪床来说,其导水率在95~827 mm/h范围内变化,总孔隙度变化范围为38.8%~47.2%,而通气孔隙度(在-3 kPa水势下)为0.9%~24.6%,毛管孔隙度(在-3 kPa水势下)为17.7%~42.1%。结果表明,排水速率和通气孔隙度与毛管孔隙度的平衡主要受沙的粒径大小的影响,起决定作用的是粒径最大和最小的沙所占的比例,而容重、总孔隙度和抗剪切强度取决于沙的均一性。当沙粒较圆且较为光滑时,坪床材料孔隙度趋向减少。沙表面越粗糙,坪床抗剪切能力就越强,而沙对坪床硬度的作用不显著。     

Feline immunodeficiency virus neurotropism: evidence that astrocytes and microglia are the primary target cells.

To investigate the neuropathogenesis of feline immunodeficiency virus (FIV) infection in vitro, we have utilized three populations of cultured feline neural cells (astrocytes, microglia, brain endothelium) to assess the relative susceptibility to FIV infection, ability to produce viral antigens, and effects of infection on cell survival. Astrocytes appeared to be the most susceptible to infection, followed by microglia, whereas brain endothelial cells were relatively resistant to infection. Astrocyte infection resulted in syncytium formation and cell death, while microglial cells remained persistently and productively infected, without obvious cytopathic effects. These results suggest that FIV entry into the central nervous system probably does not occur via infected endothelium and that both astrocytes and microglia are more likely target cells for the virus.     

Congenital dyserythropoiesis and progressive alopecia in Polled Hereford calves: hematologic, biochemical, bone marrow cytologic, electrophoretic, and flow cytometric findings.

Congenital dyserythropoiesis with dyskeratosis is a slow, progressive, and often fatal disease in Polled Hereford calves. Affected calves have a macrocytic normochromic anemia with a mild reticulocytosis. Studies indicate that calves are hyperferremic with increased saturation of serum total iron binding capacity, which rules out iron deficiency as a cause. Other secondary causes of dyserythropoiesis, including cobalamin and folate deficiencies, are unlikely because serum cobalamin and folate levels of affected calves were normal. Virus isolation was negative, and failure to identify bovine retroviral antigens or antibodies from several calves suggested that viral agents were not involved. Bone marrow cytologic findings were similar to those in congenital hereditary dyserythropoiesis in humans and included occasional multinucleate cells, internuclear chromatin bridging between nuclei of partially divided cells, and, more frequently, irregular nuclear shapes and chromatin patterns. DNA content and cell cycle distribution of erythroid cells appeared normal, and no electrophoretic abnormalities were detected in erythrocyte membrane proteins. The Polled Hereford syndrome is similar in many ways to type I congenital dyserythropoiesis in humans and may be an appropriate biomedical model for studying erythroid proliferation during dyserythropoiesis.     

Clinical and pathologic features of parvoviral diarrhea in pound-source dogs

From June 1980 through May 1982, 161 pound-source dogs that developed diarrhea while being used in research were evaluated to determine whether canine parvovirus (CPV) type 2 was the etiologic agent. Evaluation included notation of clinical signs, determination of serum CPV-specific immunoglobulin (Ig) M and IgG titers, virus isolation attempts, and histologic examination of tissues. Criteria for diagnosis of canine parvoviral enteritis were serum CPV-specific IgM antibodies, isolation of CPV from feces, and histologic evidence of intestinal crypt cell necrosis. Upon arrival, 67 clinically normal pound-source dogs were evaluated to determine the prevalence of fecal shedding of CPV and to determine their antibody titers to CPV. Parvovirus was not isolated from any of these dogs, although 76% had IgG antibodies and 3% had IgM antibodies. Of the 161 dogs with diarrhea, 40 (25%) had parvoviral enteritis. Of dogs with parvoviral enteritis, 71% had IgG antibodies and 68% had IgM antibodies. Canine parvovirus was isolated from 18 dogs. Serum IgG antibodies were found in 85% of dogs with diarrhea due to other causes. The geometric mean titer of IgG antibodies to CPV was not significantly different among the 3 groups. Clinical signs that appeared significantly (P less than 0.05) more often in dogs with parvoviral enteritis included bloody diarrhea, anorexia, fever (greater than or equal to 39.4 C), and leukopenia (WBC less than 6,000/mm3). Cases occurred throughout the year, without apparent seasonal variation. The duration between arrival and onset of diarrhea was significantly (P less than 0.05) shorter for dogs with parvoviral enteritis.(ABSTRACT TRUNCATED AT 250 WORDS)     

The importance of Campylobacter jejuni to the meat industry: a review

Campylobacter jejuni is a microorganism that only recently has been implicated in gastroenteritis in humans. As appropriate methods used for detection of the bacterium have been developed, the rates of illness caused by the pathogen were found to approach or surpass those attributed to Salmonella. Substantial evidence has been gathered to document that the route for human infection is through the ingestion of adulterated food and drink. Some slaughter animals harbor this potential pathogen among the intestinal flora and, consequently, transfer of the organism to carcasses and to the resulting meat products does occur. The most frequently implicated meat is poultry, with an incidence of recovery of C. jejuni from the store-bought poultry meat reported to be at least 50%. Red meat from slaughter animals have also yielded this bacterium from carcasses, but at lower incidence levels. Foodborne disease has been associated most frequently with the ingestion of raw milk, but poultry, hamburger, and other foods have all been implicated as potential sources. However, cause and effect relating the presence of C. jejuni in meat and human gastroenteritis has not been demonstrated. Additional research is needed to determine whether C. jejuni isolated from meat causes gastroenteritis and whether all strains of the organism are virulent. Recognition of C. jejuni as a potential meatborne pathogen by the meat industry is necessary, and appropriate sanitary practices to prevent passage of the organism through meat products should be implemented.