Improvised Inguinal Junctional Tourniquets: Recommendations From the Special Operations Combat Medical Skills Sustainment Course.

Effectively and rapidly controlling significant junctional hemorrhage is an important effort of Tactical Combat Casualty Care (TCCC) and can potentially contribute to greater survival on the battlefield. Although the US Food and Drug Administration (FDA) has approved labeling of four devices for use as junctional tourniquets, many Special Operations Forces (SOF) medics do not carry commercially marketed junctional tourniquets. As part of ongoing educational improvement during Special Operations Combat Medical Skills Sustainment Courses (SOCMSSC), the authors surveyed medics to determine why they do not carry commercial tourniquets and present principles and methods of improvised junctional tourniquet (IJT) application. The authors describe the construction and application of IJTs, including the use of available pressure delivery devices and emphasizing that successful application requires sufficient and repetitive training.

Travel Distance and Compliance to Haemodialysis in an Urban Setting in Sarawak

Discussion: Our noncompliance rate is comparable to previous Malaysian studies. SGH is located in the centre of Kuching City with good road access. Despite this, some patients still face travel issues slightly different from other states in Malaysia. A 5km travel via boat or village lane is more challenging than a 5 km travel on tar road. Further studies looking at this issue for rural haemodialysis patients would enable better planning for future dialysis centres. Conclusion: Travel distance is a significant factor for noncompliance to haemodialysis in Sarawak General Hospital, Kuching.

A magneto-optic probe for magnetic fluctuation measurements.

Results from a proof-of-principle experiment are presented that demonstrate it is possible to construct a completely optical, robust, and compact probe capable of spatially resolved measurements of magnetic field fluctuations smaller than 1 G over a frequency range of 1 Hz-8 MHz in a plasma. In contrast to conventional coil probes, the signal strength is independent of fluctuation frequency and the measurement technique is immune to electrostatic pickup. The probe consists of a high Verdet constant crystal, two polarizers, optical fibers, and a photodetector.

Increased upstream ionization due to formation of a double layer.

We report observations that confirm a theoretical prediction that formation of a current-free double layer in a plasma expanding into a chamber of larger diameter is accompanied by an increase in ionization upstream of the double layer. The theoretical model argues that the increased ionization is needed to balance the difference in diffusive losses upstream and downstream of the expansion region. In our expanding helicon source experiments, we find that the upstream plasma density increases sharply at the same antenna frequency at which the double layer appears.

Comparison of gridded energy analyzer and laser induced fluorescence measurements of a two-component ion distribution.

We present ion velocity distribution function (IVDF) measurements obtained with a five grid retarding field energy analyzer (RFEA) and IVDF measurements obtained with laser induced fluorescence (LIF) for an expanding helicon plasma. The ion population consists of a background population and an energetic ion beam. When the RFEA measurements are corrected for acceleration due to the electric potential difference across the plasma sheath, we find that the RFEA measurements indicate a smaller background to beam density ratio and a much larger parallel ion temperature than the LIF. The energy of the ion beam is the same in both measurements. These results suggest that ion heating occurs during the transit of the background ions through the sheath and that LIF cannot detect the fraction of the ion beam whose metastable population has been eliminated by collisions.

Varying Ti-6Al-4V surface roughness induces different early morphologic and molecular responses in MG63 osteoblast-like cells.

Osteoblast response to Ti implants depends not only on the chemistry of the implant but also on the physical properties of the implant surface, such as microtopography and roughness. This study was undertaken to examine early changes in cell morphology and gene expression during the early phase of osteoblast interaction with titanium alloy (Ti-6Al-4V) surfaces of two different roughnesses. MG63 osteoblast-like cells were cultured for 2, 6, 24, and 72 h on smooth (Ra=0.18+/-0.03 microm) and rough (Ra=2.95+/-0.23 microm) Ti-6Al-4V surfaces. Changes in cell proliferation were assessed by measuring cell number after 72 h in culture. Morphological characteristics were observed by scanning electron microscopy after 2, 6, and 24 h of culture. Changes in gene expression for extracellular signal-regulated kinase 2 (Erk2), type I collagen (alpha2[I] collagen), phospholipase C-gamma2 (Plc-gamma2), and beta-actin were measured by RT-PCR after 6 and 24 h in culture. Cell number was significantly higher on the smooth surface. In scanning electron micrographs, cells on smooth Ti-6Al-4V were spherical and raised up from the surface after 2 h in culture. In contrast, cells on the rough surface adopted an irregular, elongated shape that spanned across pits in the surface. At 24 h, cells on the smooth surface had flattened, become elongate, and covered the surface. In contrast, cells on the rough surface appeared more differentiated in shape and the margins of the cells were irregular, with many processes extending out, following the contour of the surface. Of the genes examined, only Erk2 and beta-actin showed a change in expression with surface roughness. Both genes were upregulated (p<0.05) on the rough surface at 6 h. These results indicate that Ti-6Al-4V surface roughness affects osteoblast proliferation, morphology, and gene expression, and that these effects can be measured after periods as short as 2-6 h.

1alpha,25(OH)2D3 causes a rapid increase in phosphatidylinositol-specific PLC-beta activity via phospholipase A2-dependent production of lysophospholipid.

1alpha,25(OH)(2)D(3) activates protein kinase C (PKC) in rat growth plate chondrocytes via mechanisms involving phosphatidylinositol-specific phospholipase C (PI-PLC) and phospholipase A(2) (PLA(2)). The purpose of this study was to determine if 1alpha,25(OH)(2)D(3) activates PI-PLC directly or through a PLA(2)-dependent mechanism. We determined which PLC isoforms are present in the growth plate chondrocytes, and determined which isoform(s) of PLC is(are) regulated by 1alpha,25(OH)(2)D(3). Inhibitors and activators of PLA(2) were used to assess the inter-relationship between these two phospholipid-signaling pathways. PI-PLC activity in lysates of prehypertrophic and upper hypertrophic zone (growth zone) cells that were incubated with 1alpha,25(OH)(2)D(3), was increased within 30s with peak activity at 1-3 min. PI-PLC activity in resting zone cells was unaffected by 1alpha,25(OH)(2)D(3). 1beta,25(OH)(2)D(3), 24R,25(OH)(2)D(3), actinomycin D and cycloheximide had no effect on PLC in lysates of growth zone cells. Thus, 1alpha,25(OH)(2)D(3) regulation of PI-PLC enzyme activity is stereospecific, cell maturation-dependent, and nongenomic. PLA(2)-activation (mastoparan or melittin) increased PI-PLC activity to the same extent as 1alpha,25(OH)(2)D(3); PLA(2)-inhibition (quinacrine, oleyloxyethylphosphorylcholine (OEPC), or AACOCF(3)) reduced the effect of 1alpha,25(OH)(2)D(3). Neither arachidonic acid (AA) nor its metabolites affected PI-PLC. In contrast, lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE) activated PI-PLC (LPE>LPC). 1alpha,25(OH)(2)D(3) stimulated PI-PLC and PKC activities via Gq; GDPbetaS inhibited activity, but pertussis toxin did not. RT-PCR showed that the cells express PLC-beta1a, PLC-beta1b, PLC-beta3 and PLC-gamma1 mRNA. Antibodies to PLC-beta1 and PLC-beta3 blocked the 1alpha,25(OH)(2)D(3) effect; antibodies to PLC-delta and PLC-gamma did not. Thus, 1alpha,25(OH)(2)D(3) regulates PLC-beta through PLA(2)-dependent production of lysophospholipid.

Informed consent for total hip arthroplasty: does a written information sheet improve recall by patients?

OBJECTIVE: To ascertain whether a written information sheet is acceptable to patients and improves recall of the consent interview. DESIGN: Prospective randomised controlled study using questionnaires, comparing a group of patients given information in a written sheet with appropriate explanation to a group given verbal information alone. SETTING: A specialist orthopaedic surgery unit. PATIENTS: The test group was 126 patients undergoing revision or primary total hip arthroplasty; 65 patients were given information verbally, 61 patients were given written information. OUTCOME MEASURE: Patients' recall of information given, tested with a questionnaire completed on admission (mean of 18 days later). RESULTS: The patients receiving written information scored significantly higher (48% correct answers) than the patients receiving verbal information (38% correct answers). CONCLUSIONS: Written information sheets contribute to the process of informed consent. As patients' recall of information is generally poor, the sheets may also be useful medicolegally, as a permanent record of what was discussed.

1alpha,25-dihydroxyvitamin D(3) and 24R,25-dihydroxyvitamin D(3) modulate growth plate chondrocyte physiology via protein kinase C-dependent phosphorylation of extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase.

Membrane-mediated increases in protein kinase C (PKC) activity and PKC-dependent physiological responses of growth plate chondrocytes to vitamin D metabolites depend on the state of endochondral maturation; 1alpha,25-dihydroxyvitamin D(3) [1alpha,25-(OH)(2)D(3)] regulates growth zone (GC) cells, whereas 24R,25-(OH)(2)D(3) regulates resting zone (RC) cells. Different mechanisms, including protein kinase A signaling, mediate the effects of 1alpha,25-(OH)(2)D(3) and 24R,25-(OH)(2)D(3) on PKC, suggesting that different mechanisms may also regulate any MAPK involvement in the physiological responses. This study used confluent cultures of rat costochondral chondrocytes as a model. 1alpha,25-(OH)(2)D(3) stimulated MAPK specific activity in GC in a time- and dose-dependent manner, evident within 9 min. 24R,25-(OH)(2)D(3) stimulated MAPK in RC; increases were dose dependent, occurred after 9 min, and were greatest at 90 min. In both cells the effect was due to ERK1/2 activation (p42 > p44 in GC; p42 = p44 in RC). MAPK activation was dependent on PKC, but not protein kinase A. The effect of 1alpha,25-(OH)(2)D(3) required phospholipase C, and the effect of 24R,25-(OH)(2)D(3) required phospholipase D. Inhibition of cyclooxygenase activity reduced the effect of 1alpha,25-(OH)(2)D(3) on MAPK in GC and enhanced the effect of 24R,25-(OH)(2)D(3) in RC. Based on MAPK inhibition with PD98059, ERK1/2 MAPK mediated the effect of 24R,25-(OH)(2)D(3) on [(3)H]thymidine incorporation and [(35)S]sulfate incorporation by RC, but only partially mediated the effect of 1alpha,25-(OH)(2)D(3) on GC. ERK1/2 was not involved in the regulation of alkaline phosphatase specific activity by either metabolite. This paper supports the hypothesis that 1alpha,25-(OH)(2)D(3) regulates the physiology of GC via rapid membrane-mediated signaling pathways, and some, but not all, of the response to 1alpha,25-(OH)(2)D(3) is via the ERK family of MAPKs. In contrast, 24R,25-(OH)(2)D(3) exerts its effects on RC via PKC-dependent MAPK. Whereas 1alpha,25-(OH)(2)D(3) increases MAPK activity via phospholipase C and increased prostaglandin production, 24R,25-(OH)(2)D(3) increases MAPK via phospholipase D and decreased prostaglandin production. The cell specificity, metabolite stereospecificity, and the dependence on PKC argue for the participation of membrane receptors for 1alpha,25-(OH)(2)D(3) and 24R,25-(OH)(2)D(3) in the regulation of ERK1/2 in the growth plate.

Rat costochondral chondrocytes produce 17beta-estradiol and regulate its production by 1alpha,25(OH)(2)D(3).

Prior studies have shown that 17beta-estradiol (17beta-E(2)) regulates growth plate chondrocyte maturation and differentiation. This study examines the hypothesis that 17beta-E(2) is a local regulator of rat costochondral growth plate chondrocytes by determining whether these cells express aromatase mRNA and enzyme activity, produce 17beta-E(2), and regulate 17beta-E(2) production by vitamin D(3) metabolites in a gender-specific and cell-maturation-dependent manner. Aromatase gene expression was assessed by reverse transcription-polymerase chain reaction (RT-PCR) and northern analysis of total RNA from male and female chondrocytes. Aromatase specific activity was measured in cell layer lysates of confluent male and female rat costochondral resting zone (RC) and growth zone (GC) cartilage cells that had been treated for 24 h with 1alpha, 25(OH)(2)D(3), 24R,25(OH)(2)D(3), or transforming growth factor (TGF)-beta1. 17beta-E(2) released into the culture media of treated cells was measured by radioimmunoassay (RIA). Female RC cells expressed the highest levels of aromatase mRNA compared with male RC cells and both male and female GC cells. Aromatase activity was present in male and female cells and was 1.6 times greater in female RC cells than female GC cells; male RC and GC cells displayed comparable levels. All cultures produced 17beta-E(2), with a 2.5-fold greater production by female RC cells than female GC cells or either cell type from male rats. Treatment of cultures with 1alpha,25(OH)(2)D(3) caused a dose-dependent increase in 17beta-E(2) production by female RC (1.5-fold greater than control cells) and female GC (threefold greater than control cells) cells. In contrast, 1alpha,25(OH)(2)D(3) had no effect on male GC cells and increased production in male RC cells by only 10% at the highest concentration of 1alpha,25(OH)(2)D(3) used. Neither 24R, 25(OH)(2)D(3) nor TGF-beta1 had an effect on 17beta -E(2) production. These results support our hypothesis and indicate that 17beta-E(2) is most likely a local regulator of rat costochondral growth plate chondrocytes.

Characterization of PGE(2) receptors (EP) and their role as mediators of 1alpha,25-(OH)(2)D(3) effects on growth zone chondrocytes.

Growth plate chondrocyte function is modulated by the vitamin D metabolite 1alpha,25-(OH)(2)D(3) via activation of protein kinase C (PKC). In previous studies with cells derived from prehypertrophic and upper hypertrophic zones of rat costochondral cartilage (growth zone cells), inhibition of prostaglandin production with indomethacin caused a decrease in the stimulation of PKC activity, suggesting that changes in prostaglandin levels mediate the 1alpha,25-(OH)(2)D(3)-dependent response in these cells. Growth zone cells also respond to PGE(2) directly, indicating that prostaglandins act as autocrine or paracrine regulators of chondrocyte metabolism in the growth plate. The aim of the present study was to identify which PGE(2) receptor subtypes (EP) mediate the effects of PGE(2) on growth zone cells. Using primers specific for EP1-EP4, reverse transcription-polymerase chain reaction (RT-PCR) amplified EP1 and EP2 cDNA in a RT-dependent manner. In parallel experiments, we used EP subtype-specific agonists to examine the role of EP receptors in 1alpha,25-(OH)(2)D(3)-mediated cell proliferation and differentiation. 17-Phenyl-trinor-PGE(2) (PTPGE(2)), an EP1 agonist, decreased [3H]-thymidine incorporation in a dose-dependent manner and augmented the 1alpha,25-(OH)(2)D(2)-induced inhibition of [3H]-thymidine incorporation. PTPGE(2) also caused significant increases in proteoglycan production, as measured by [35S]-sulfate incorporation, and alkaline phosphatase specific activity. 1alpha,25-(OH)(2)D(3)-induced alkaline phosphatase activity was only slightly stimulated by PTPGE(2). In contrast, 1alpha,25-(OH)(2)D(3)-induced PKC activity was synergistically increased by PTPGE(2), whereas EP1 antagonists SC-19220 and AH6809 inhibited PKC activity in a dose-dependent manner. The EP2, EP3 and EP4 agonists had no effect on the various cell-induced responses measured. EP1 receptor-induced responses were blocked by the phospholipase C inhibitor U73122, and reduced by PKA inhibitors. EP1 receptor-induced PKC activity was insensitive to pertussis toxin or choleratoxin but blocked by the G-protein inhibitor GDPbetaS, suggesting the involvement of G(q). These results suggest that the EP1 receptor subtype mediates various PGE(2)-induced cellular responses in growth zone chondrocytes leading to decreased proliferation and enhanced differentiation, as well as the effect of 1alpha,25-(OH)(2)D(3) on cellular maturation.

Effects of 1alpha,25-(OH)(2)D(3) on rat growth zone chondrocytes are mediated via cyclooxygenase-1 and phospholipase A(2).

1alpha,25-(OH)(2)D(3) mediates its effects on growth zone chondrocytes via rapid membrane-associated events as well as through traditional nuclear receptor mechanisms. The membrane-associated signaling pathways include rapid production of diacylglycerol and activation of protein kinase C (PKC), as well as activation of phospholipase A(2) (PLA(2)), increased production of arachidonic acid, and increased production of prostaglandins. This study examined the roles of PLA(2) and cyclooxygenase (Cox) in the mechanism of action of 1alpha,25-(OH)(2)D(3) in these cells to determine whether one or both enzymes catalyze the rate limiting step and whether constitutive or inducible Cox is involved. Cultures were incubated with 1alpha,25-(OH)(2)D(3) for 9 min to measure PKC or for 24 h to measure physiological responses ([(3)H]-thymidine incorporation, alkaline phosphatase specific activity, [(35)S]-sulfate incorporation). Based on RT-PCR and Northern blot analysis, growth zone chondrocytes expressed mRNAs for both Cox-1 and Cox-2 and neither Cox was modulated by 1alpha,25-(OH)(2)D(3). To examine the role of Cox, the cultures were also treated with resveratrol (a specific inhibitor of Cox-1), NS-398 (a specific inhibitor of Cox-2), or indomethacin (a general Cox inhibitor). The results showed that Cox-1 inhibition reduced the 1alpha,25-(OH)(2)D(3)-dependent effects on proliferation, differentiation, and matrix production, whereas inhibition of Cox-2 only had an effect on proliferation. The effects of Cox inhibition were not rate limiting, based on experiments in which PLA(2) was activated with melittin or inhibited with quinacrine. However, at least part of the action of 1alpha,25-(OH)(2)D(3) was regulated by metabolism of arachidonic acid to prostaglandins. This supports the hypothesis that 1alpha,25-(OH)(2)D(3) exerts its effects via more than one signaling pathway and that these pathways are interrelated via the modulation of PLA(2) as a rate-limiting step. PKC regulation may occur at multiple stages in the signal transduction cascade. J. Cell. Biochem. Suppl. 36: 32-45, 2001.

Regulation of phospholipase D (PLD) in growth plate chondrocytes by 24R,25-(OH)2D3 is dependent on cell maturation state (resting zone cells) and is specific to the PLD2 isoform.

Many of the effects of 1alpha,25-(OH)2D3 and 24R,25-(OH)2D3 on costochondral chondrocytes are mediated by the protein kinase C (PKC) signal transduction pathway. 1alpha,25-(OH)2D3 activates PKC in costochondral growth zone chondrocytes through a specific membrane receptor (1alpha,25-mVDR), involving rapid increases in diacylglycerol via a phospholipase C (PLC)-dependent mechanism. 24R,25-(OH)2D3 activates PKC in resting zone chondrocytes. Although diacylglycerol is increased by 24R,25-(OH)2D3, PLC is not involved, suggesting a phospholipase D (PLD)-dependent mechanism. Here, we show that resting zone and growth zone cells express mRNAs for PLD1a, PLD1b, and PLD2. Both cell types have PLD activity, but levels are higher in resting zone cells. 24R,25-(OH)2D3, but not 24S,25-(OH)2D3 or 1alpha,25-(OH)2D3, stimulates PLD activity in resting zone cells within 3 min via nongenomic mechanisms. Neither 1alpha,25-(OH)2D3 nor 24R,25-(OH)2D3 affected PLD in growth zone cells. Basal and 24R,25-(OH)2D3-stimulated PLD were inhibited by the PLD inhibitors wortmannin and EDS. Inhibition of phosphatidylinositol 3-kinase (PI 3-kinase), PKC, phosphatidylinositol-specific PLC (PI-PLC), and phosphatidylcholine-specific PLC (PC-PLC) had no effect on PLD activity. Thus, 24R,25-(OH)2D3 stimulates PLD, and PI 3-kinase, PI-PLC and PKC are not involved, whereas PLD is required for stimulation of PKC by 24R,25-(OH)2D3. Pertussis toxin, GDPbetaS, and GTPgammaS had no effect on 24R,25-(OH)2D3-dependent PLD when added to cell cultures, indicating that G-proteins are not involved. These data show that PKC activation in resting zone cells is mediated by PLD and suggest that a functional 24R,25-(OH)2D3-mVDR is required. The results also support the conclusion that the 24R,25-(OH)2D3-responsive PLD is PLD2, since this PLD isoform is G-protein-independent.

Expression and production of stathmin in growth plate chondrocytes is cell-maturation dependent.

Growth plate cartilage is comprised of linear columns of chondrocytes with the least differentiated cells at one end and the terminally differentiated cells at the other end. Rat costochondral chondrocytes can be divided into the resting cell zone (reserve cell zone), which contains relatively immature chondrocytes (RC cells), and the phenotypically more mature prehypertrophic and upper hypertrophic cell zones, which together may be termed the growth zone chondrocytes (GC cells). When grown separately in monolayer culture, they continue to express their zone-specific phenotype, providing a model for assessing cell-maturation-dependent expression of molecules associated with differentiation. Stathmin (also called prosolin, Op18, p19, 19K, and others) is a highly conserved, phosphorylated cytosolic protein with apparent ubiquitous expression. Although its exact function is unknown, stathmin is considered to be a messenger phosphorylated protein, it plays a role in tubulin stability, and it may participate in both general and specific regulatory pathways. One uniform observation is that the expression of stathmin protein decreases in all cells as they become more terminally differentiated in culture. There have been no published data regarding stathmin expression and production in chondrocytes. This study was based on the hypothesis that stathmin exists in chondrocytes and that the mRNA and protein levels decline in the GC cell with respect to the RC cell. Stathmin mRNA levels were determined and quantitated by reverse transcription-polymerase chain reaction (RT-PCR) and northern blots. Protein levels were determined using immunoblots. It was found that stathmin exists in chondrocytes and that RC cells express approximately twice the level of mRNA and protein to that found in GC cells. The results support the hypothesis and suggest that the level of stathmin expression and production in culture is related to the level of differentiation of RC and GC cells in vivo.

24R,25-(OH)(2)D(3) mediates its membrane receptor-dependent effects on protein kinase C and alkaline phosphatase via phospholipase A(2) and cyclooxygenase-1 but not cyclooxygenase-2 in growth plate chondrocytes.

Recent studies have shown that 24R,25-(OH)(2)D(3) mediates its effects on growth plate chondrocytes via membrane receptors. This study examined the roles of phospholipase A(2) (PLA(2)) and cyclooxygenase (Cox) in the mechanism of action of 24R, 25-(OH)(2)D(3) in resting zone chondrocytes in order to determine whether the activity of one or both enzymes provides a regulatory checkpoint in the signaling pathway resulting in increased protein kinase C (PKC) activity. We also determined whether constitutive or inducible Cox is involved. Cultures were incubated with 24R, 25-(OH)(2)D(3) for 90 min to measure PKC or for 24 h to measure physiological responses ([(3)H]-thymidine incorporation, alkaline phosphatase-specific activity, [(35)S]-sulfate incorporation). Based on RT-PCR and Northern blot analysis, resting zone chondrocytes express mRNAs for both Cox-1 and Cox-2. Levels of mRNA for both proteins were unchanged from control levels after a 24-h incubation with 24R,25-(OH)(2)D(3). To examine the role of Cox, the cultures were also treated with resveratrol (a specific inhibitor of Cox-1), NS-398 (a specific inhibitor of Cox-2), or indomethacin (a general Cox inhibitor). Cox-1 inhibition resulted in effects on proliferation, differentiation, and matrix production typical of 24R, 25-(OH)(2)D(3). In contrast, inhibition of Cox-2 had no effect, indicating that 24R,25-(OH)(2)D(3) exerts its effects via Cox-1. Inhibition of Cox-1 also blocked 24R,25-(OH)(2)D(3)-dependent increases in PKC. Activation of PLA(2) with melittin inhibited 24R, 25-(OH)(2)D(3)-dependent stimulation of PKC, and inhibition of PLA(2) with quinacrine stimulated PKC in response to 24R, 25-(OH)(2)D(3). Inclusion of resveratrol reduced the melittin-dependent inhibition of PLA(2) and caused an increase in quinacrine-stimulated PLA(2) activity. Metabolism of arachidonic acid to leukotrienes is not involved in the response to 24R, 25-(OH)(2)D(3) because inhibition of lipoxygenase had no effect. The effect of 24R,25-(OH)(2)D(3) was specific because 24S,25-(OH)(2)D(3), the biologically inactive stereoisomer, failed to elicit a response from the cells. These results support the hypothesis that 24R, 25-(OH)(2)D(3) exerts its effects via more than one signaling pathway and that these pathways are interrelated via the modulation of PLA(2). PKC regulation may occur at multiple stages in the signal transduction cascade.

Assessment of learning ability and behaviour in low birthweight lambs following intrauterine growth restriction.

The present study used behavioural tasks to assess learning ability and behaviour in postnatal lambs, and to examine the effects of low birthweight (LBW) and age on subsequent performance. It was hypothesized that intrauterine growth restriction (IUGR) and LBW lead to learning and behavioural deficits in the early postnatal period. IUGR and LBW were induced by umbilico-placental embolization from 120 days of gestational age (g.a.) to the onset of labour. Behavioural studies were performed on 6 LBW and 6 control lambs between 2 and 6 weeks after birth. LBW lambs were born at 139+/-1 days g.a. (2.4+/-0.2 kg) and control lambs were born at 149+/-1 days g.a. (4.5+/-0.4 kg). Three tasks were used to assess the learning ability and behaviour of the lambs: a simple maze, an obstacle course, and a T-maze. LBW lambs took longer to complete the simple maze at all ages, and made a greater number of errors at Week 1 of testing compared to control lambs; the total trial duration and number of errors decreased with age for both groups. In the obstacle course, the times taken to complete the first and third trials were used for analysis; a decrease in trial time and the number of errors from Trial 1 to Trial 3 were indications of the lamb's ability to learn how to negotiate the objects within the course. LBW lambs recorded longer trial durations for the first trial at Week 5 of testing, and for the third trial at Week 4. LBW lambs made more errors for the first trial at Week 5 of testing than control lambs. In the T-maze, there was no significant effect of treatment or age. It was concluded that differences between the groups may have been the result of LBW lambs being prematurely born. The value of these tasks in the assessment of learning ability and behaviour in young lambs is discussed.

Amino acid digestibilities in different samples of wheat shorts for growing pigs.

An experiment was carried out to investigate the variability in apparent ileal amino acid (AA) digestibilities in simulated samples of wheat shorts consisting of different proportions of wheat bran (WB), wheat shorts (WS), and wheat flour (WF), hereafter referred to as wheat fractions. The proportions of WS, WB, and WF and the NDF content (DM basis) of the wheat fractions were as follows: A, 70% WS, 30% WB, and 42.3% NDF; B, 85% WS, 15% WB, and 41.8% NDF; C, 100% WS and 41.3% NDF; D, 85% WS, 15% WF, and 35.2% NDF; and E, 70% WS, 30% WF, and 29.5% NDF. Six barrows, average initial BW of 37.2 kg, fitted with a simple T-cannula at the distal ileum, were fed one of six experimental diets according to a 6 x 6 Latin square design. Six diets were formulated to contain 17% CP (as-fed basis). Diets A, B, C, D, and E contained 17.53% soybean meal (SBM), which contributed 50% of the CP in these diets. The wheat fractions contributed the remaining 50% of the CP in these diets. Diet F contained 35.05% SBM, which was the sole source of dietary CP. Chromic oxide was used as the digestibility marker. During the first experimental period, the daily dietary allowance was provided at a rate of 5% (wt/wt) of the average BW. Thereafter, the daily dietary allowance was increased by 100 g at each successive period. Each experimental period comprised 12 d. Following a 7-d adaptation period, feces were collected for 48 h and ileal digesta for a total of 24 h. The apparent ileal digestibilities of AA in the wheat fractions were calculated using the difference method. The digestibilities were usually lowest in the wheat fractions containing WB and highest in those containing no WB. The average of the digestibilities of the indispensable AA was 63.5% for wheat fraction A, which contained 30% WB, and 71.9% for wheat fraction C, which did not contain WB. There were no differences (P > .05) in lysine digestibilities among the wheat fractions, which ranged from 54.7 to 64.1%. Of the indispensable AA, with the exception of arginine, lysine, and methionine, the apparent ileal digestibility values of AA were negatively correlated (P < .05) with the NDF content in the wheat fractions.

Carcass traits and reproductive development at the onset of lay in two lines of female turkeys.

A study was conducted comparing ovary and oviduct development following photostimulation in two lines of turkey breeder stocks (female line and male line). Birds were euthanatized for assessment of reproductive organ morphology at 3-d intervals following photostimulation (203 d of age) to 245 d and on the day following their first oviposition. The age at first oviposition was similar for both lines. Male line birds were 3 to 4 kg heavier than female line birds throughout the study, but had lower abdominal fat pad weights when expressed as a percentage of BW. Female line birds had significantly more total carcass lipid as a percentage of BW than male line birds (24.76 vs 22.79%, respectively). Male line birds had significantly more large ovarian follicles with a greater proportion in a triple or greater hierarchical arrangement at first egg. To determine the incidence of unreconciled ovulations (presumed to be internally ovulated follicles and defined as ovulations occurring prior to first oviposition), postovulatory follicles on the ovary were reconciled with observed ovipositions and the developing eggs that were in the oviduct at the time of study. On average, male line hens had 3.0 unreconciled postovulatory follicles at first egg, whereas the female line hens had 1.6. The incidence of birds with physical remnants of internal ovulation was correlated (r = 0.44) to the number of unreconciled ovulations. The developing oviduct of the female line birds reached its mature weight (84.8 g) 3 d earlier than the ovary did. The developing ovary and oviduct of the male line hens reached their mature weights on the same day. The development of the male line oviduct is seemingly accelerated relative to that of the ovary, resulting in lost ovulations early in lay.