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The disorders of consciousness refer to clinical conditions that follow a severe head injury. Patients diagnosed as in a vegetative state lack awareness, while patients diagnosed as in a minimally conscious state retain fluctuating awareness. However, it is a challenge to accurately diagnose these disorders with clinical assessments of behavior. To improve diagnostic accuracy, neuroimaging-based approaches have been developed to detect the presence or absence of awareness in patients who lack overt responsiveness. For the small subset of patients who retain awareness, brain-computer interfaces could serve as tools for communication and environmental control. Here we review the existing literature concerning the sensory and cognitive abilities of patients with disorders of consciousness with respect to existing brain-computer interface designs. We highlight the challenges of device development for this special population and address some of the most promising approaches for future investigations.

P-selectin on platelets and endothelial cells and E-selectin on endothelial cells are leukocyte receptors that recognize lineage-specific carbohydrates on neutrophils and monocytes. The proposed ligands for these receptors contain the Le(x) core and sialic acid. Since other investigators have shown that both E-selectin and P-selectin bind to sialylated Le(x), we evaluated whether E-selectin and P-selectin recognize the same counter-receptor on leukocytes. The interaction of HL60 cells with Chinese hamster ovary (CHO) cells expressing P-selectin or E-selectin was studied. To determine whether a protein component is required in addition to sialyl Le(x) for either P-selectin or E-selectin recognition, HL60 cells or neutrophils were digested with proteases, including chymotrypsin, elastase, proteinase Glu-C, ficin, papain, or thermolysin. Cells treated with these proteases bound E-selectin but not P-selectin. Fucosidase or neuraminidase treatment of HL60 cells markedly decreased binding to both E-selectin- and P-selectin-expressing CHO cells. Growth of HL60 cells in tunicamycin inhibited the ability of these cells to support P-selectin-mediated binding and, to a lesser extent, E-selectin-mediated binding. Purified P-selectin inhibited CHO:P-selectin binding to HL60 cells, but incompletely inhibited CHO:E-selectin binding to HL60 cells. However, purified soluble E-selectin inhibited CHO:P-selectin and CHO:E-selectin binding to HL60 cells equivalently and completely. COS cells, unable to bind to E-selectin or P-selectin, bound E-selectin but not P-selectin upon transfection with alpha-1,3-fucosyltransferase or alpha-1,3/1,4-fucosyltransferase. Similarly, LEC 11 cells expressing sialyl Le(x) bound E-selectin- but not P-selectin-expressing CHO cells. Sambucus nigra lectin, specific for the sialyl-2,6 beta Gal/GalNAc linkage, inhibited P-selectin but not E-selectin binding to HL60 cells. Although sialic acid and Le(x) are components of the P-selectin ligand and the E-selectin ligand, these results indicate that the ligands are related, having overlapping specificities, but are structurally distinct. A protein component containing sialyl Le(x) in proximity to sialyl-2,6 beta Gal structures on the P-selectin ligand may contribute to its specificity for P-selectin.

The inflammatory cytokine interleukin-1 (IL-1) has profound actions in the brain, causing neuronal cell death and exacerbating brain damage. While circulating levels are normally low, IL-1 can be produced on the vascular side of the brain endothelium, and within the brain. The naturally occurring IL-1 receptor antagonist has been administered peripherally in a Phase II trial in acute stroke patients; understanding how IL-1 and IL-1 receptor antagonist penetrate the brain is, therefore, of considerable importance.An in vitro blood-brain barrier model was generated by co-culture of porcine brain microvascular endothelial cells with astrocytes. The mechanisms of transcellular transport of IL-1beta and IL-1 receptor antagonist were characterized in this model, using endocytosis inhibitors and IL-1 receptor-blocking antibodies.Transcellular IL-1beta and IL-1 receptor antagonist transport was temperature-dependent and IL-1beta was transported with higher affinity than IL-1 receptor antagonist. IL-1beta inhibited IL-1 receptor antagonist transport more potently than IL-1 receptor antagonist inhibited IL-1beta transport. Transport of IL-1beta and IL-1 receptor antagonist was not via adsorptive-mediated endocytosis, although inhibition of microtubule assembly significantly attenuated transport of both cytokines. An antibody directed to the type II IL-1 receptor significantly reduced IL-1beta transport.These results are consistent with IL-1 and IL-1 receptor antagonist being transported across cultured cerebromicrovascular endothelial cells and suggest that IL-1beta transport may occur via a type II IL-1 receptor-dependent mechanism. Understanding IL-1 transport into the brain may have benefits, particularly in enhancing penetration of IL-1 receptor antagonist into the brain.

Two single mutants and the corresponding double mutant of beta-lactamase I from Bacillus cereus 569/H were constructed and their kinetics investigated. The mutants have Lys-73 replaced by arginine (K73R), or Glu-166 replaced by aspartic acid (E166D), or both (K73R + E166D). All four rate constants in the acyl-enzyme mechanism were determined for the E166D mutant by the methods described by Christensen, Martin & Waley [(1990) Biochem. J. 266, 853-861]. Both the rate constants for acylation and deacylation for the hydrolysis of benzylpenicillin were decreased about 2000-fold in this mutant. In the K73R mutant, and in the double mutant, the rate constants for acylation were decreased about 100-fold and 10,000-fold respectively. All three mutants also had lowered values for the rate constants for the formation and dissociation of the non-covalent enzyme-substrate complex. The specificities of the mutants did not differ greatly from those of wild-type beta-lactamase, but the hydrolysis of cephalosporin C by the K73R mutant gave ‘burst’ kinetics.

An experiment with a completely randomized 2-by-3 factorial design was used to study the effects of ochratoxin A (OA; 0 and 4 mg of OA per kg) and supplemental L-phenylalanine (Phe; .0%, .8%, and 2.4% of Phe) in the diets of 3-wk-old broilers. Diets based on ground yellow corn and dehulled soybean meal were fed from Day 1 to 3 wk of age. A total of 240 male Hubbard-by-Hubbard broilers were randomly placed in battery brooders with 10 birds per pen. Each treatment was replicated 4 times. The parameters measured included mortality, BW, feed conversion, and relative organ weight. Broilers receiving OA weighed less and had poorer feed conversions than birds not receiving OA. For broilers receiving OA, the relative weights (grams of organ weight per 100 g of BW) of the liver, proventriculus, gizzard, and heart increased, while the relative weight of the bursa decreased. Supplemental Phe decreased the relative weight of the liver and increased the relative weight of the gizzard and heart. The regression slopes for Phe at 4 mg of OA per kg of diet were significantly different from 0 for BW, the relative weights of the kidney, spleen, and pancreas and approached significance for mortality (P = .065). In the absence of supplemental Phe, 42.5% of the birds died during the study when the dose level was 4 mg of OA per kg of diet. However, when Phe was supplemented at .8 and 2.4%, only 12.5 and 15.0% of the birds died, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

"The purpose of this study is to track and contrast the patterns of local concentration and deconcentration in nonmetropolitan America between 1950 and 1996. We consider the growth of places by initial size as well as the growth of population living in the countryside or in unincorporated hamlets.... To determine how widespread and consistent the trends are, we compare patterns of growth by nearness to metropolitan areas, and by region of the country. We also examine differences among a subset of nonmetropolitan places distinguished by the primary socioeconomic character of their county. Using a detailed data file from the 1990 census, we are able to give some consideration to commuting."

We have identified a mutant of the human G-protein Cdc42Hs, R66E, that fails to form a detectable complex with the GDP-dissociation inhibitor RhoGDI in cell-free systems or in intact cells. This point mutant is prenylated, binds guanine nucleotide and interacts with GTPase-activating protein in a manner indistinguishable from wild-type Cdc42Hs. Immunofluorescence localization studies revealed that this RhoGDI-binding-defective mutant is found predominantly in the Golgi apparatus, with a staining pattern similar to that of the wild-type protein. However, unlike wild-type Cdc42Hs, which is distributed in both the microsomal membrane and cytosolic fractions, studies using differential centrifugation show that prenylated R66E Cdc42Hs is found exclusively in association with lipid bilayers. Additionally, whereas the overexpression of RhoGDI results in an apparent translocation of wild-type Cdc42Hs from the Golgi apparatus into the cytosol, identical RhoGDI-overexpression conditions do not alter the Golgi localization of the R66E mutant. Furthermore, overexpression of this RhoGDI-binding-defective mutant of Cdc42Hs seems to activate redistribution of the actin cytoskeleton and filopodia formation in fibroblasts in a manner indistinguishable from the wild-type protein. Taken together, these results suggest that the interaction of Cdc42Hs with RhoGDI is not essential for proper membrane targeting of nascent prenylated Cdc42Hs in mammalian cells; neither is this interaction an essential part of the mechanism by which Cdc42Hs activates filopodia formation. However, it does seem that redistribution of Cdc42Hs to the cytosolic compartment is absolutely dependent on RhoGDI interaction.

We used microsatellite DNA markers to genotype chicks in 10 broods of lek-breeding sage grouse, Centrocercus urophasianus, whose mothers' behaviour was studied by radio-tracking and observing leks. Previous behavioural studies suggested that almost all matings are performed by territorial males on leks and that multiple mating is rare. Two broods (20%) were sired by more than one male. Genetic analyses of the broods of eight females that visited an intensively studied lek were consistent with behavioural observations. Four females observed mating produced singly sired broods and males other than the individual observed copulating were excluded as sires for most or all of their chicks. Territorial males at the study lek were excluded as sires of broods of four other females that visited the lek but were not observed mating there. Radio-tracking suggested that two of these females mated at other leks. Our results confirm the reliability of mating observations at leks, but do not rule out a possible unseen component of the mating system.

The receptor for leukemia inhibitory factor (LIF) consists of two polypeptides, the LIF receptor and gp130. Agonist stimulation has been shown previously to cause phosphorylation of gp130 on serine, threonine, and tyrosine residues. We found that gp130 fusion proteins were phosphorylated exclusively on Ser-782 by LIF- and growth factor-stimulated 3T3-L1 cell extracts. Ser-780 was required for phosphorylation of Ser-782 but was not itself phosphorylated. Ser-782 is located immediately N-terminal to the di-leucine motif of gp130, which regulates internalization of the receptor. Transient expression of chimeric granulocyte colony-stimulating factor receptor (G-CSFR)-gp130(S782A) receptors resulted in increased cell surface expression in COS-7 cells and increased ability to induce vasoactive intestinal peptide gene expression in IMR-32 neuroblastoma cells when compared with expression of chimeric receptors containing wild-type gp130 cytoplasmic domains. These results identify Ser-782 as the major phosphorylated serine residue in human gp130 and indicate that this site regulates cell surface expression of the receptor polypeptide.

The catalytic (C) subunit of cAMP-dependent protein kinase requires two distinct surfaces to form a stable complex with its physiological inhibitors, the regulatory (R) subunits and the heat-stable protein kinase inhibitors. In addition to a substrate-like segment that is common to both inhibitors, R requires a peripheral recognition site, PRS2. This surface is comprised of the essential phosphorylation site, Thr-197, His-87, Trp-196, and several surrounding basic residues. To probe the role of Trp-196 in the recognition of R, Trp-196 was replaced with Arg and Ala. Although both rC(W196A) and rC(W196R) were inhibited readily with cAMP-free R, they failed to form an inhibited holoenzyme complex with native R under conditions in which wild-type holoenzyme formed readily. Pairing rC(W196R) with mutant forms of R lacking domain B or having defects in cAMP binding sites A or B highlighted the importance of the conformation of R, and, in particular, the accessibility of site A. One of these mutants, rR(R333K), having a defect in cAMP binding site B formed a stable complex with rC(W196R) in the absence of cAMP. However, unlike wild-type holoenzyme, this complex was active.

Since a basic surface on the catalytic (C) subunit of cAMP-dependent protein kinase is important for binding to the regulatory (R) subunit, acidic residues in R were sought that might contribute to R-C interaction. Using differential labeling by a water-soluble carbodiimide (Buechler, T. A., and Taylor, S. S. (1990) Biochemistry 29, 1937-1943), seven specific carboxylates in RIalpha were identified that were protected from chemical modification in the holoenzyme; each was then replaced with Ala. Of these, rRI(E15A/E106A/D107A)), rRI(E105A), rRI(D140A), rRI(E143A), and rRI(D258A) all were defective in holoenzyme formation and define negative electrostatic surfaces on RIalpha. An additional conserved carboxylate, Glu101 in RIalpha and the equivalent, Glu99 in RIIalpha were mutated to Ala. Replacement of Glu101 had no effect while rRII(E99A) was very defective. RIalpha and RIIalpha thus differ in the molecular details of how they recognize C. Unlike wild-type RI, two additional mutants, rRI(D170A) and rRI(K242A), inhibited C-subunit stoichiometrically in the presence of cAMP and show increases in both on- and off-rates. Asp170, which contributes directly to the hydrogen bonding network in cAMP-binding site A, thus contributes also to holoenzyme stability.

P-selectin is an integral membrane glycoprotein on stimulated platelets and endothelial cells that serves as a receptor for leukocytes. To estimate the density of P-selectin in membranes necessary to support adhesion, we incorporated purified P-selectin at varying concentrations into phospholipid bilayers that encapsulated glass microspheres. Maximal binding of these lipospheres to HL60 cells, a P-selectin ligand-expressing cell line, was approached at a P-selectin density of about 100 molecules per microns 2; half-maximal binding was observed at about 50 to 60 molecules per microns 2. Compatible results were obtained with P-selectin expressed on Chinese hamster ovary cells. The P-selectin density on stimulated platelets was estimated to be 150 to 200 molecules/microns 2. To identify the domains of P-selectin required for HL60 cell binding, chimeras of P-selectin and L-selectin were stably expressed in Chinese hamster ovary cells and clones that expressed the chimeras at the estimated physiologic density were selected. Chimeras containing the P-selectin lectin and epidermal growth factor (EGF) domains or the lectin, EGF, and short consensus repeats bound HL60 cells equivalently, but a chimera containing the P-selectin lectin domain alone bound HL60 cells much less well. These results indicate that at a physiologically relevant P-selectin density on membrane surfaces, the lectin, and EGF domains of P-selectin are together required for optimal leukocyte binding.

P-selectin on platelets and endothelial cells and E-selectin on endothelial cells are leukocyte receptors that recognize lineage-specific carbohydrates on neutrophils and monocytes. The proposed ligands for these receptors contain the Le(x) core and sialic acid. Since other investigators have shown that both E-selectin and P-selectin bind to sialylated Le(x), we evaluated whether E-selectin and P-selectin recognize the same counter-receptor on leukocytes. The interaction of HL60 cells with Chinese hamster ovary (CHO) cells expressing P-selectin or E-selectin was studied. To determine whether a protein component is required in addition to sialyl Le(x) for either P-selectin or E-selectin recognition, HL60 cells or neutrophils were digested with proteases, including chymotrypsin, elastase, proteinase Glu-C, ficin, papain, or thermolysin. Cells treated with these proteases bound E-selectin but not P-selectin. Fucosidase or neuraminidase treatment of HL60 cells markedly decreased binding to both E-selectin- and P-selectin-expressing CHO cells. Growth of HL60 cells in tunicamycin inhibited the ability of these cells to support P-selectin-mediated binding and, to a lesser extent, E-selectin-mediated binding. Purified P-selectin inhibited CHO:P-selectin binding to HL60 cells, but incompletely inhibited CHO:E-selectin binding to HL60 cells. However, purified soluble E-selectin inhibited CHO:P-selectin and CHO:E-selectin binding to HL60 cells equivalently and completely. COS cells, unable to bind to E-selectin or P-selectin, bound E-selectin but not P-selectin upon transfection with alpha-1,3-fucosyltransferase or alpha-1,3/1,4-fucosyltransferase. Similarly, LEC 11 cells expressing sialyl Le(x) bound E-selectin- but not P-selectin-expressing CHO cells. Sambucus nigra lectin, specific for the sialyl-2,6 beta Gal/GalNAc linkage, inhibited P-selectin but not E-selectin binding to HL60 cells. Although sialic acid and Le(x) are components of the P-selectin ligand and the E-selectin ligand, these results indicate that the ligands are related, having overlapping specificities, but are structurally distinct. A protein component containing sialyl Le(x) in proximity to sialyl-2,6 beta Gal structures on the P-selectin ligand may contribute to its specificity for P-selectin.

An experiment with a completely randomized 2-by-3 factorial design was used to study the effects of ochratoxin A (OA; 0 and 4 mg of OA per kg) and supplemental L-phenylalanine (Phe; .0%, .8%, and 2.4% of Phe) in the diets of 3-wk-old broilers. Diets based on ground yellow corn and dehulled soybean meal were fed from Day 1 to 3 wk of age. A total of 240 male Hubbard-by-Hubbard broilers were randomly placed in battery brooders with 10 birds per pen. Each treatment was replicated 4 times. The parameters measured included mortality, BW, feed conversion, and relative organ weight. Broilers receiving OA weighed less and had poorer feed conversions than birds not receiving OA. For broilers receiving OA, the relative weights (grams of organ weight per 100 g of BW) of the liver, proventriculus, gizzard, and heart increased, while the relative weight of the bursa decreased. Supplemental Phe decreased the relative weight of the liver and increased the relative weight of the gizzard and heart. The regression slopes for Phe at 4 mg of OA per kg of diet were significantly different from 0 for BW, the relative weights of the kidney, spleen, and pancreas and approached significance for mortality (P = .065). In the absence of supplemental Phe, 42.5% of the birds died during the study when the dose level was 4 mg of OA per kg of diet. However, when Phe was supplemented at .8 and 2.4%, only 12.5 and 15.0% of the birds died, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Phenylalanine was evaluated for its ability to protect broiler chickens from the toxic effects of ochratoxin A (OA). A completely randomized 2-by-3 factorial design was utilized consisting of 0, .8, and 2.4% supplemental L-phenylalanine (Phe) and of 0 and 4 mg of OA per kg of diet. The basal diet contained 14% protein. Broilers were raised in battery brooders to 3 wk of age, when blood was collected and various hematological parameters were determined. The health status of the broilers was evaluated by assaying serum for various enzyme activities and metabolites using an automated, clinical chemistry analyzer. Adding OA to the broiler diets resulted in an increased concentration of serum hemoglobin as well as increased activity for cholinesterase and gamma glutamyl transferase but in decreased activity for aspartate amino transferase, lactate dehydrogenase, and alkaline-phosphatase activity as well as decreased concentrations of total triglyceride and of inorganic phosphorus. Supplemental Phe decreased the concentrations of hemoglobin and serum glucose. The regression slopes for Phe at 4 mg of OA per kg of diet were significant for uric acid, creatinine, total protein, albumin, and cholesterol suggesting that supplemental Phe improved the health status of the broilers fed diets containing OA with respect to these parameters.

Dimethyl sulphoxide (DMSO) reductase activity increased at the end of the growth cycle of Saccharomyces cerevisiae NCYC 240 on complex medium. On defined medium, DMSO reductase and thioredoxin reductase activities and thioredoxin were all elevated in cultures limiting in nitrogen, but not in nitrogen-sufficient cultures. In nitrogen limiting cultures it was also shown that the reduction of DMSO (measured as disappearance of [14C] from the medium) was much increased compared with conditions of nitrogen excess. This applied whether ammonium or glutamate was the limiting nitrogen source. When methionine was used as the limiting nitrogen source, DMSO reduction was higher still. Methionine-limited cells accumulated [17C] methionine much more rapidly than did cells from methionine-sufficient cultures, and [14C] methionine sulphoxide could be identified in the cells after 1 min incubation with labelled methionine. It is concluded that DMSO reductase activity is controlled by nitrogen catabolite repression and may be involved in methionine uptake by yeast. The amino nitrogen content of wort will in consequence have an important effect on levels of dimethylsulphide (DMS) produced during fermentation.

The health status of broilers fed diets with varying protein contents in the presence of ochratoxin A (OA) were evaluated using clinical-chemistry techniques for blood analysis. A completely randomized, 3 × 4 factorial design was utilized: 14, 18, 22, and 26% of dietary protein and 0, 2, and 4 mg/kg of OA. The broilers were raised to 3 wk of age, at which time blood was collected and various hematological parameters were evaluated. The serum was analyzed for various enzyme activities and for concentrations of metabolites and minerals using an automated, clinical-chemistry analyzer and an atomic-absorption spectrophotometer. Adding OA to the diets of broilers decreased the hemoglobin concentration, corpuscular volume, and the activity of serum alkaline and phosphatase but increased the activity of gamma-glutamyl transferase. Adding protein to the diet increased the activity of the serum aspartate aminotransferase, creatine kinase, and alkaline phosphatase. Adding OA to the diet of broilers decreased the concentrations of serum total protein, as well as the concentrations of albumen and cholesterol and increased the concentrations of serum creatinine and uric acid. The concentrations of serum total protein, albumin, urea nitrogen, and triglyceride were increased by adding protein to the diet. The concentrations of calcium, potassium, and inorganic phosphorus in the serum decreased when OA was added to the diet; but the concentrations of calcium and potassium content in the serum increased along with dietary protein. A regression analysis suggested that dietary protein was synergistic toward OA with regard to the blood levels of cholinesterase, lactate dehydrogenase, and glucose. But an antagonistic relationship was noted between dietary protein and OA for blood levels of total protein, albumin, cholesterol, calcium, and potassium.

The distribution of calving times in a population of Red deer on the Isle of Rhum, Inner Hebrides, between 1971 and 1976 is described. Two-thirds of calves were born during a three-week period beginning in the last week of May, though calving extended from early May to late August. Except in 1976, when calving occurred late, the timing of births was similar in all years. Variation in calving time within years resulted from (i) individual differences in calving time, (ii) late conception in hinds which failed to conceive at first oestrus, and (iii) the effect of previous reproductive history: on average, hinds calved one week later after rearing a calf in the previous winter. Gestation lengths of wild hinds were longer than in a captive group. This may have been due to overestimation of a proportion of gestation lengths in wild hinds, but supplementary feeding could also have shortened gestation length in captive animals.

Ten patients with intracranial lesions, anaesthetized with thiopentone and nitrous oxide (70%) in oxygen (30%) received etomidate 0.2 mg kg-1 i.v. Ventilation was controlled in each patient. Intracranial pressure (i.c.p.) and mean arterial pressure (m.a.p.) were recorded. I.c.p. decreased significantly in all patients (0.01 greater than P greater than 0.001). Although PaCO2 decreased during the period of measurement, the extent and time-course of this change suggested that it was not mainly responsible for changes in i.c.p. M.a.p. decreased in most patients, but the decrease was statistically significant only at 3 and 4 min after the administration of etomidate (0.05 greater than P greater than 0.02). The changes in cerebral perfusion pressure (c.p.p.) and heart rate were not clinically or statistically significant. We conclude that etomidate can be used for the induction of anaesthesia in patients with intracranial space-occupying lesions without increasing i.c.p. or seriously reducing c.p.p.

Seventy-six severely head-injured patients, 67% of whom had Glasgow Coma scores of five or less on admission, were managed according to an intensive treatment regime which included controlled hyperventilation (under full muscular paralysis), high-dose steroids, dehydrating agents, diuretics and hypnotics (Althesin and thiopentone). Intracranial pressure (ICP) was measured throughout the period of controlled ventilation. Treatment was directed to keeping the mean ICP below 25-30 mmHg and to the prevention of increases in ICP during chest physiotherapy and other noxious stimulation. Six months after injury 46% of patients had died and 4% were vegetative survivors, whilst 43% had made a good recovery or were only moderately disabled. Features associated with worse than average prognosis were: low coma score, pupillary abnormalities, respiratory dysrhythmia and ICP greater than 30 mmHg. Spontaneous hyperventilation was a relatively good initial feature. These results support the employment of intensive care in severely head-injured patients, particularly those with diffuse brain injury.

During fermentation, yeast reduced [14C] dimethyl sulphoxide (DMSO) to yield radioactive dimethyl sulphide (DMS) even under conditions in which no net formation of DMS could be demonstrated by GLC analysis. It was confirmed that most DMS is produced during fermentation of lager worts at 8°C.

Disadvantages associated with the use of ventricular catheters for the prolonged measurement of intracranial pressure have resulted in the search for an alternative technique. Measurement of pressure from the extradural space is one such possibility, but widespread acceptance of this procedure has been limited by the technical difficulties associated with this measurement and lack of information on the relationship between cerebrospinal fluid and extradural pressures. A study to investigate this relationship and to develop a simple and effective technique for measuring extradural pressure is described.

alpha-Amylase isozymes 1 and 2 isolated from germinated barley seeds have been crystallized by the hanging- or sitting-drop vapor diffusion technique. Crystals of alpha-amylase 2 suitable for x-ray diffraction analysis were grown at pH 6.7 and 22 degrees C from a solution of 1 mM calcium chloride, 10 mM MES, and 16% saturated ammonium sulfate. The space group is trigonal P3121 (or P3221) with unit cell dimensions a = b = 135.20 A, c = 79.63 A, and probably two molecules per asymmetric unit.alpha-Amylase isozymes 1 and 2 isolated from germinated barley seeds have been crystallized by the hanging- or sitting-drop vapor diffusion technique. Crystals of alpha-amylase 2 suitable for x-ray diffraction analysis were grown at pH 6.7 and 22 degrees C from a solution of 1 mM calcium chloride, 10 mM MES, and 16% saturated ammonium sulfate. The space group is trigonal P3121 (or P3221) with unit cell dimensions a = b = 135.20 A, c = 79.63 A, and probably two molecules per asymmetric unit.

Browne, F. J., and Browne, J. C. McClure (1955). Postgraduate Obstetrics and Gynaecology, 2nd ed., p. 236. Butterworth, London. Burton-Brown, J. R. C. (1949). J. Obstet. Gvnaec. Brit. Emp., 56, 847. Davis, M. E., and Boynton, M. W. (1942). Amer. J. Obstet. Gynec, 43, 775. Dewhurst, C. J. (1952). Lancet, 2, 746. Dutton, W. A. C. (1958). /. Obstet. Gynaec. Brit. Emp., 65, 315. Elwin, P. M. (1960). Brit. med. J., 1, 1569. Fraser, A. C, and Tatford, E. P. W. (1961). Lancet, 2, 126. Greenhill, J. P. (1960). Obstetrics, 12th ed., p. 307. Saunders, Philadelphia and London. Kimbell, N. (1958). Brit. med. J., 1, 203. Left", M. (1929). Amer. J. Obstet. Gynec, 18, 868. Lloy , H. N. (1949). Proc. roy. Soc. Med., 42, 1. Martin, J. D., and Dumoulin, J. G. (1953). Brit. med. J., 1, 643. Ministry of Health (1960). Report of Confidential Enquiries into Maternal Deaths in England and Wales, 1955-7. H.M.S.O., London. Moir, J. Chassar (1956). Munro Kerr's Operative Obstetrics, 6th ed., p. 48. Bailli?re, Tindall and Cox, London. Morris, W. I. C. (1959). British Obstetric and Gynaecological Practice, edited by Sir Eardley Holland and Aleck Bourne, 2nd ed., p. 809. Nixon, W. C. W. (1955). W. Afr. med. J., 4, 52. Picton, F. C. R. (1951). /. Obstet. Gynaec. Brit. Emp., 58, 764. Stabler, F. (1957). Brit. med. J., 2, 217. Williams, J. Whitridge (1924). Obstetrics, 5th ed., p. 336. Appleton, New York and London.

The exercise program presented uses exercises to quickly build up the patient's facial muscles and confidence. It is an active process, and the patient must be encouraged to do the exercise to get the full and satisfactory effect. The dental office staff should be encouraged to follow this program too. The results will be noticed, and they can support the patients in doing these exercises. Smiles do much to improve the environment we work and live in.

The Nation spent $163 billion for health care in fiscal year 1977 or $737 per person, according to preliminary figures compiled by the Health Care Financing Administration. This figure was 12 percent higher than spending for such purposes in the previous 12 months and represented an 8.8-percent share of the GNP. Public spending, which financed 42 percent of all health care in 1977, increased 11 percent while private spending rose 13 percent. Spending for hospital care went up 14 percent to $68.4 billion, and the total spent for physicians' services ($32.2 billion) reflected a 13-percent rise. Third-party payments financed 70 percent of all personal health care in the country.

According to preliminary estimates of the Nation's health spending in fiscal year 1975, health expenditures reached $118.5 billion, or $547 per person. Total health spending showed a 14-percent rise, significantly higher than the increase in 1974 when price controls in the health industry were in effect for most of the year. The acceleration of health spending during 1975 was accompanied by a slackening in the growth of the gross national product. Expenditures for this purpose, as a share of the GNP, thus rose significantly to 8.3 percent. Public spending grew two and one-half times as fast as private spending in 1975, mainly because of the continuing expansion of Medicare and Medicaid. Third parties financed an estimated two-thirds of all personal health care spending, with the government share 40 percent and that of private insurance 27 percent.

The health status of broilers fed diets with varying protein contents in the presence of ochratoxin A (OA) were evaluated using clinical-chemistry techniques for blood analysis. A completely randomized, 3 x 4 factorial design was utilized: 14, 18, 22, and 26% of dietary protein and 0, 2, and 4 mg/kg of OA. The broilers were raised to 3 wk of age, at which time blood was collected and various hematological parameters were evaluated. The serum was analyzed for various enzyme activities and for concentrations of metabolites and minerals using an automated, clinical-chemistry analyzer and an atomic-absorption spectrophotometer. Adding OA to the diets of broilers decreased the hemoglobin concentration, corpuscular volume, and the activity of serum alkaline and phosphatase but increased the activity of gamma-glutamyl transferase. Adding protein to the diet increased the activity of the serum aspartate aminotransferase, creatine kinase, and alkaline phosphatase. Adding OA to the diet of broilers decreased the concentrations of serum total protein, as well as the concentrations of albumen and cholesterol and increased the concentrations of serum creatinine and uric acid. The concentrations of serum total protein, albumin, urea nitrogen, and triglyceride were increased by adding protein to the diet. The concentrations of calcium, potassium, and inorganic phosphorus in the serum decreased when OA was added to the diet; but the concentrations of calcium and potassium content in the serum increased along with dietary protein. A regression analysis suggested that dietary protein was synergistic toward OA with regard to the blood levels of cholinesterase, lactate dehydrogenase, and glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

An experiment with a completely randomized 3 x 4 factorial design was used to study the effects of ochratoxin A (0, 2, and 4 mg/kg) and protein (14, 18, 22, and 26%) in three-wk-old broilers. The diets were based on ground yellow corn and dehulled soybean meal. Four hundred and eighty Hubbard x Hubbard broilers were randomly placed in battery brooders, with 10 birds per pen. Each treatment was replicated four times. Body weight increased with rising levels of protein, and decreased with rising levels of ochratoxin A (OA). The efficiency of feed utilization was improved in broilers fed 22 and 26% protein, compared with broilers fed 14 and 18% protein. The efficiency of feed utilization was lower for the birds fed 4 mg/kg of OA, compared with broilers fed 0 and 2 mg/kg of OA, respectively. Using OA increased the relative weight of the liver, kidney, spleen, pancreas, proventriculus, gizzard, and heart and also significantly decreased the relative weight of the bursa of fabricius. A significant interaction between OA and protein was seen in terms of the relative weight of the liver, pancreas, and gizzard, indicating that the rising protein levels spared the OA effect on those organs. Mortality was highest among the broilers fed 4 mg/kg of OA. Protein regression coefficients (beta's) were positive with respect to 21-day body weight and were negative for the feed:gain ratio and mortality, suggesting that protein provided beneficial effects.

This report of health care spending in fiscal year 1975 reveals that of the $103.2 billion spent by the Nation for personal health care, 15 percent was spent for those under age 19, 56 percent for persons aged 19-64, and 29 percent for those aged 65 or older. The average health care bill for the oldest group was $1,360; it was $472 for the intermediate age group and $212 for the young. Third-party payments met 71 percent of the aged group's health care expense and 66 percent of the health expenditures of persons under age 65. Public funds paid for one-fourth of the health expenses of the young, nearly one-third of the health bills of those aged 19-64, and two-thirds of those of the aged. Medicare alone paid 72 percent of the hospital expense for the aged and 54 percent of their doctor bills. The average direct payment by the consumer amounted to $390 for those aged 65 and older and $128 for persons under age 65.

Summary Two patients with spinal epidural abscess, but with different neurological outcomes, are presented. The pathogenesis, clinical features and current treatment are reviewed. The need for early diagnosis is once again stressed.

SUMMARY Intracranial pressure (i.c.p.) and mean arterial pressure (m.a.p.) were studied in 20 patients during the induction of anaesthesia for craniotomy. Tubocurarine was administered as the muscle relaxant and either thiopentone or Althesin for the induction of anaesthesia. No significant differences were found in the i.c.p. changes with induction, intubation or pharyngeal packing, between the thiopentone and the Althesin groups. Except for two patients (one in each group) the increases in i.c.p. associated with intubation were small. In these two patients moderate increases from normal values to 28 and 37 mm Hg were recorded, but in one of these patients coughing and straining followed intubation. Marked decreases in m.a.p. were noted in both groups, but the recovery of m.a.p. was significantly more rapid in the Althesin group. Only two patients had i.c.p. values greater than 20 mm Hg before operation and in neither did i.c.p. increase above control values during induction and intubation. Packing the pharynx produced minimal changes in i.c.p. in all patients.

alpha-Amylase isozymes 1 and 2 isolated from germinated barley seeds have been crystallized by the hanging- or sitting-drop vapor diffusion technique. Crystals of alpha-amylase 2 suitable for x-ray diffraction analysis were grown at pH 6.7 and 22 degrees C from a solution of 1 mM calcium chloride, 10 mM MES, and 16% saturated ammonium sulfate. The space group is trigonal P3121 (or P3221) with unit cell dimensions a = b = 135.20 A, c = 79.63 A, and probably two molecules per asymmetric unit.

The United States spent an estimated $287 billion for health care in 1981 (Figure 1), an amount equal to 9.8 percent of the Gross National Product (GNP). Highlights of the figures that underly this estimate include the following: Health care expenditures continued to grow at a rapid rate in 1981, at a time when the economy as a whole exhibited sluggish growth. The 9.8 percent share of the GNP was a dramatic increase from the 8.9 percent share seen just two years earlier. Health care expenditures amounted to $1,225 per person in 1981 (Table 1). Of that amount, $524, or 42.7 percent, came from public funds. Hospital care accounted for 41.2 percent of total health care spending in 1981 (Table 2). These expenditures increased 17.5 percent from 1980, to a level of $118 billion. Spending for the services of physicians increased 16.9 percent to $55 billion--19.1 percent of all health care spending. Public sources provided 42.7 percent of the money spent on health in 1981, including Federal payments of $84 billion and $39 billion in State and local government funds (Table 3). All third parties combined--private health insurers, governments, private charities, and industry--financed 67.9 percent of the $255 billion in personal health care in 1981 (Table 4), covering 89.2 percent of hospital care services, 62.1 percent of physicians' services, and 41.3 percent of the remainder (Table 5). Direct patient payments for health care reached $82 billion in 1981, accounting for 32.1 percent of all personal health care expenses (Table 6). Consumers and their employers paid another $73 billion in premiums to private health insurers, $67 billion of which was returned in the form of benefits. Outlays for health care benefits by the Medicare and Medicaid programs totaled $73 billion, including $42 billion for hospital care. The two programs combined paid for 28.6 percent of all personal health care in the nation (Table 7).

Outlays for health care in the nation reached $212.2 billion in calender year 1979--12.5 percent higher than in 1978, according to preliminary figures compiled by the Health Care Financing Administration. This estimate represented $943 per person in the United States and was equal to 9.0 percent of the Gross National Product. This latest report in the annual series representing national health expenditures provides detailed estimates of health care spending by type of service and method of financing.

Of the $120.4 billion spent by the Nation for personal health care in fiscal year 1976, 29% was spent for those aged 65 or older, 15% for those under age 19, and the remaining 56% for those aged 19-64. The average health bill reached $1,521 for the aged, $547 for the intermediate age group, and $249 for the young. Public funds financed 68% of the health expenses of the aged with Medicare and Medicaid together accounting for 59%. Private sources paid 74% of the health expenses of the young and 70% of the expenses of those aged 19-64. Third-party payments met 65% of the health expenditures of all those under age 65.