Molecular phylogeny of the New World monkeys (Platyrrhini, primates) based on two unlinked nuclear genes: IRBP intron 1 and epsilon-globin sequences

Nuclear sequences of the 1.8 kilobase (kb) long intron 1 of the interstitial retinol-binding protein gene (IRBP), previously determined for 11 of the 16 extant genera of New World monkeys (superfamily Ceboidea, infraorder Platyrrhini), have now been determined for the remaining 5 genera. The maximum parsimony trees found, first with IRBP sequences alone and then with tandemly combined IRBP and epsilon-globin gene sequences from the same species, supported a provisional cladistic classification with the following clusters. Subtribes Callitrichina (Callithrix, Cebuella), Callimiconina (Callimico), Leontopithecina (Leontopithecus) and Saguina (Saguinus) constitute subfamily Callitrichinae, and subfamilies Callitrichinae, Aotinae (Aotus), and Cebinae (Cebus, Saimiri) constitute family Cebidae. Subtribes Chiropotina (Chiropotes, Cacajao) and Pitheciina (Pithecia) constitute tribe Pitheciini; and tribes Pitheciini and Callicebini (Callicebus) constitute subfamily Pitheciinae. Subtribes Brachytelina (Brachyteles, Lagothrix) and Atelina (Ateles) constitute tribe Atelini, and tribes Atelini and Alouattini (Alouatta) constitute subfamily Atelinae. The parsimony results were equivocal as to whether Pitheciinae should be grouped with Atelinae in family Atelidae or have its own family Pitheciidae. The cladistic groupings of extant ceboids were also examined by different stochastic evolutionary models that employed the same stochastic process of nucleotide substitutions but alternative putative phylogenetic trees on which the nucleotide substitutions occurred. Each model, i.e., each different tree, predicted a different multinomial distribution of nucleotide character patterns for the contemporary sequences. The predicted distributions that were closest to the actual observed distributions identified the best fitting trees. The cladistic relationships depicted in these best fitting trees agreed in almost all cases with those depicted in the maximum parsimony trees.     

Role for macrophage inflammatory protein-2 in lipopolysaccharide-induced lung injury in rats

Macrophage inflammatory protein-2 (MIP-2) is a C-X-C chemokine that possesses chemotactic activity for neutrophils. Rat MIP-2 was cloned and expressed as a 7.9-kDa peptide that exhibited dose-dependent neutrophil chemotactic activity at concentrations from 10 to 250 nM. Rabbit polyclonal Ab to the 7.9-kDa peptide showed reactivity by western blot analysis and suppressed its in vitro chemotactic activity. Cross-desensitization chemotaxis experiments suggested that the chemotactic responses elicited by MIP-2 and the related chemokine, cytokine-induced neutrophil chemoattractant, may be mediated through a common receptor. Also, chemotactic responses to human GRO-alpha were blocked by exposure of human neutrophils to either GRO-alpha or rat MIP-2, suggesting conservation of this receptor-mediated response. After LPS instillation into rat lung, mRNA for MIP-2 was up-regulated in a time-dependent manner, peaking at 6 h. MIP-2 protein was detected in bronchoalveolar lavage fluids of these animals and a significant amount of chemotactic activity present in these fluids was attributed to MIP-2. On the basis of intrapulmonary instillation of Ab to MIP-2, neutrophil accumulation in lungs after airway instillation of LPS was found to be MIP-2-dependent. These data indicate that MIP-2 plays a significant role in LPS-induced inflammatory response in rat lungs and is required for the full recruitment of neutrophils.     

Roasted soybeans, blood meal, and tallow as sources of fat and ruminally undegradable protein in the diets of lactating cows

The effect of roasted soybeans, blood meal, and tallow as sources of fat and RUP for lactating dairy cows was studied. Forty-five cows, blocked by age, calving date, and milk yield during the previous lactation, were assigned randomly to the following treatments (ingredient in the DM, RUP as a percentage of CP, and fat in the DM, respectively): 1) soybean meal (16, 35, and 3.2%), 2) whole roasted soybeans (18, 40, and 6.2%), 3) ground roasted soybeans (18, 40, and 6.2%), 4) blood meal (2.7, 40, and 3.2%), and 5) blood meal plus tallow (2.7 and 3, 40, and 6.2%). Diets were fed from wk 3 to 18 of lactation and consisted of 20% alfalfa silage, 30% corn silage, and 50% concentrate. The DMI of blood meal and whole roasted soybean diets was about 11% lower than DMI of the soybean meal diet. Milk yield (38.4 kg/d) and milk fat percentage (3.37%) were similar among diets. The roasted soybean diets resulted in the lowest milk protein percentage. Less than 2.7% blood meal might be advisable for diets fed to high yielding dairy cows to avoid reduced DMI.     

Decreased interleukin-2 production in murine acute pancreatitis: potential for immunomodulation

BACKGROUND & AIMS: The role of the cytokine interleukin 2 (IL-2) has long been recognized as central to normal immunologic function and defense against infection after burns and trauma, but little effort has been directed towards its role in acute pancreatitis (AP), which also has a high mortality related to sepsis. This study investigated the potential role of IL-2 in mice with diet-induced AP. METHODS: AP was induced in mice by 10 days of feeding a choline-deficient, ethionine-supplemented diet. T-helper (CD4) cells were estimated, and T-cell mitogen-stimulated splenocyte proliferation and IL-2 production in vitro were measured on days 3, 7, and 10. RESULTS: Significant reduction in IL-2 production was found on day 3 (32%; P < 0.05) and day 10 (48%; P < 0.005). Administration of intraperitoneal lipopolysaccharide on day 10 was associated with reduced IL-2 production (P < 0.025) 4 hours later and 90% mortality in animals with AP. In vivo therapy with recombinant IL-2 improved in vitro IL-2 secretion (P < 0.05) and reduced lipopolysaccharide-induced mortality (P = 0.036). CONCLUSIONS: Murine diet-induced AP is associated with impaired immune function and increased susceptibility to sepsis and may be a valuable tool in the investigation of immunomodulation in AP.     

Corticosterone has independent effects on tissue maturation and growth in the suckling rat

Glucocorticoids are associated with reduced weight gain when used to improve pulmonary function in premature infants. However, tissue maturation is stimulated during normal development by an increase in serum glucocorticoids. We evaluated the effects of glucocorticoid treatment on tissue weight gain and the activity of specific enzymes in the suckling rat, with the hypothesis that these processes are independently regulated. Before the ontogenic surge in corticosterone, 6-d-old rat pups were implanted with a pellet to release corticosterone continuously at 0 (placebo), 48, 120, 240, or 360 micro g/d. We killed the pups at 7, 9, or 12 d of age and measured tissue weights and activities of sucrase and glutamine synthetase. Serum corticosterone concentrations were elevated with dose. Tissue weight gain was proportional to ln(e) serum corticosterone at all ages. In contrast, enzyme indices of tissue maturation did not respond to corticosterone until d9. Also, intestinal tissue was more sensitive than muscle to the effects of corticosterone on weight but less sensitive to its effects on maturation. We conclude that the immediate response, in terms of weight versus the delayed response of the enzymes and their reciprocal sensitivity in muscle and gut, indicates that these processes are independently regulated.     

Relationship among hormonal treatments, suppression of spermatogenesis, and testicular protection from chemotherapy-induced damage

To further elucidate the mechanism by which hormonal pretreatment protects the rat testis from damage by procarbazine, we investigated the relationship between the suppression of hormone levels and spermatogenesis and the recovery of spermatogenesis from stem spermatogonia. LBNF1 rats were implanted with capsules containing testosterone or testosterone plus estradiol. After hormone treatment, rats were injected with procarbazine, and recovery of spermatogenesis was assessed. Testosterone (2 cm) plus estradiol (0.5-cm) reduced serum LH levels causing intratesticular testosterone (ITT) to fall to 3% of control levels within 2 weeks, but testis weights and sperm head counts were not appreciably suppressed until 4 weeks. Two weeks' hormone pretreatment, only slightly enhanced spermatogenesis recovery, but 4 weeks markedly increased it. Testosterone (2 cm) alone produced slower suppression of spermatogenesis and less protection from procarbazine than did testosterone plus estradiol implants, despite equivalent suppression of LH and ITT. Long testosterone implants (24-cm) partially maintained ITT at 14% of control despite undetectable LH levels, prevented any decline in sperm counts, and nearly completely abrogated the protective effect of the hormone treatment. Protection appeared to be best correlated with the testis weight reduction by hormone treatment. Thus, recovery of spermatogenesis after chemotherapy is dependent on the degree of suppression of spermatogenesis caused by the reduction of ITT levels at the time of chemotherapy and likely involves cells, such as the Sertoli cells, that are both androgen-responsive and affected by the numbers of germ cells present.