Miracle-dz/UniFAR-FTUs huggingface dataset:
Ontogeny of hematological cell and biochemical profiles in maternal and fetal baboons (Papio species)

Abstract: The normal ranges of hematological cell profiles and biochemistry are documented in adult non‐pregnant, pregnant, juvenile, and neonatal baboons. Despite the extensive use of the baboon as a model for the study of various aspects of pregnancy, there is no data from paired mothers and their fetuses at different stages of gestation. Hematologic and biochemical profile data were obtained from eight non‐pregnant female baboons, 37 mothers and 38 fetal baboons at 30 ± 2, 90 ± 2, 125 ± 2, and 175 ± 2 days of gestation (mean ± range; dGA; term, 180 dGA). Changes observed in fetal and maternal blood during normal baboon pregnancy were similar to those reported in human pregnancy. The level of alkaline phosphatase was two times higher in fetal blood circulation than that reported in human pregnancy.
Intracranial pressure and ocular hemodynamics.

In owl monkeys, controlled elevation of subarachnoid pressure was produced either intracranially, in the optic nerve sheath, or in both. When intracranial pressure was elevated, orbital venous pressure became elevated, but it did not keep pace with intracranial pressure elevation, because orbital veins have anastomoses to facial veins and need not depend entirely on cavernous sinus for drainage. The central retinal vein pressure is additionally affected by pressure in optic nerve sheaths, and keeps pace with vaginal sheath pressure elevation, because anastomotic connections at the optic disc between central retinal vein and vortex vein were not sufficient to relieve fully pressure in the central retinal vein. Intraocular blood flow was slowed in regions drained by central retinal vein (retina and disc). The choroidal flow, which drains via vortex veins into orbital veins, was affected less.
Smoke exposure exacerbates an ethanol-induced defect in mucociliary clearance of Streptococcus pneumoniae.

BACKGROUND Alcoholics and smokers are particularly susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. Infection begins when pneumococci colonizing the nasopharynx are aspirated into the lower respiratory tract. The major host defense against this movement is the mucociliary clearance apparatus. Both cigarette smoke and ethanol (EtOH) exposure alter ciliary beating and protein kinase activity in the respiratory mucosa in vitro, but their effects on bacterial clearance in the intact animal have not been determined. METHODS Male Sprague Dawley rats were exposed twice daily for 12 weeks to either the smoke generated from 30 cigarettes (smoke-exposed) or room air (sham-exposed). For the last five weeks of smoke exposure, the rats were fed Lieber-DeCarli liquid diets containing 0%, 16%, 26%, or 36% EtOH calories. The rats then were infected intranasally with S. pneumoniae, and movement of the organisms into the lower respiratory tract was quantified by plate counts of the tracheas and lungs 4 hr later. Ciliary beat frequency (CBF) analysis was performed on tracheal ring explants from each animal before and after stimulation with the beta-agonist isoproterenol, and tracheal epithelial cell protein kinase C (PKC) activity was measured. RESULTS Ingestion of any of the EtOH-containing diets resulted in a dose-dependent increase in movement of S. pneumoniae into the rats' lungs. This EtOH-induced defect was augmented further by concurrent smoke exposure, although smoke exposure alone had little effect on S. pneumoniae movement. Smoke, but not EtOH exposure, activated tracheal epithelial cell PKC. Increased movement of organisms into lungs correlated with a decrease in CBF and loss of the ciliary response to isoproterenol. CONCLUSION EtOH ingestion in our model facilitated movement of S. pneumoniae into rats' lungs, a phenomenon exacerbated by concurrent smoke exposure. Furthermore, the organism's movement into the lungs correlated with a blunting of the rats' ciliary response to an established stimulus. Defects in mucociliary clearance thus may be one cause of the increased risk of pneumococcal infections in people who abuse alcohol, particularly if they also smoke.
The association of depression and anxiety with unhealthy lifestyle among United Arab Emirates adults

Dear Editor The prevalence of mental health disorders in the United Arab Emirates (UAE) has increased over the past several decades (Abou-Saleh et al. 2001). According to local estimates, approximately between 55% and 73% of patients attending primary care in the UAE suffer mental disorders (El-Rufaie & Absood, 1993). The commonest diagnoses were depressive disorders 55%, mixed anxiety-depression 13% and anxiety disorders 12%. Worldwide research showed that depression and anxiety are major causes of morbidity and mortality (Harter et al. 2003; Chapman et al. 2005; Amaddeo & Tansella, 2010) and are associated with impaired health-related quality of life and social functioning, as well as with increased risk for disability (Kivimakl et al. 2009). Recent research indicates that people with major depression or anxiety disorders particularly panic disorder, have a higher prevalence of regular smoking than those without such conditions (McCabe et al. 2004). Obesity has been associated with increased life time risk for major depression and panic disorder or agoraphobia, particularly among females (Baumeister & Harter, 2007; Carpiniello et al. 2009), and physical inactivity has been associated with depression (Allgower et al. 2001). In the meantime, exercise has been found to be an effective adjunct to the usual forms of treatment for depression, anxiety and has even a protective effect against suicide (Dunn et al. 2005; Muller et al. 2009). In this study, we examined the extent to which depression and anxiety were associated with smoking, physical inactivity and obesity among UAE adults using data from the population-based UAE health and life survey 2000 (UAEHALS 2000). To our knowledge, this is the first large population-based study to examine these associations using the Hospital Anxiety and Depression Scale (HADS; Zigmond & Snaith, 1983).
DIVERSITY IN ARBUSCULAR MYCORRHIZAL MORPHOLOGY IN SOME MEDICINAL PLANTS OF FAMILY LAMIACEAE

Present study was designed to find out the mycorrhizal status of some selected medicinal plants of family Lamiaceae growing in KPK (Khyber Pakhtunkhawa). The mycorrhizal infections were present in all studied species. Typical Arum and Paris type mycorrhiza are recorded for the first time from the family Lamiaceae. The number of studied plants with Arum type was higher than Paris type while two plants were recorded with intermediate type. Variations in the percentage of general VAM infection ranged from 55-100%.
Growth‐rate recovery of Escherichia coli cultures carrying a multicopy plasmid, by engineering of the pentose‐phosphate pathway

Expression of plasmid‐encoded genes in bacteria is the most common strategy for the production of specific proteins in biotechnological processes. However, the synthesis of plasmid‐encoded proteins and plasmid‐DNA replication often places a metabolic load (metabolic burden) into the cell's biochemical capacities that usually reduces the growth rate of the producing culture (Glick BR. Biotechnol Adv 1995;13:247–261). This metabolic burden may be related to a limited capacity of the cell to supply the extra demand of building blocks and energy required to replicate plasmid DNA and express foreign multicopy genes. Some of these required blocks are intermediaries of the pentose phosphate (PP) pathway, e.g., ribose‐5‐phosphate, erythrose‐4‐phosphate. Due to the important impact of metabolic burden on biotechnological processes, several groups have worked on developing strategies to overcome this problem, like reduction of plasmid copy number (Seo JH, Bailey JE. Biotechnol Bioeng 1985;27:1668–1674; Jones KL, Kim S, Keasling JD. Metab Eng 2000;3:328–338), chromosomal insertion of the gene which product is desired, or changing the plasmid‐coded antibiotic resistance gene (Hong Y, Pasternak JJ, Glick BR. Can J Microbiol 1995;41:624–628). However, few efforts have been attempted to overcome the reduction of growth rate due to protein over‐expression, by modifying central metabolic pathways (Chou C‐H, Bennett GN, San KY. Biotechnol Bioeng 1994;44:952–960). We constructed a high‐copy number plasmid carrying the gene for glucose‐6‐phosphate dehydrogenase, zwf, under the control of an inducible trc promoter (pTRzwf04 plasmid). By transforming a wild‐type strain and inducing with IPTG, it was possible to recover growth‐rate from 0.46 h−1 (uninduced) to 0.64 h−1 (induced). The same transformation in an Escherichia coli zwf−, allows a growth‐rate recovery from 0.43 h−1 (uninduced) to 0.62 h−1 (induced). We also studied this effect as part of a laboratory‐scale biotechnology process: production of a recombinant insulin peptide by co‐transforming E. coli JM101 strain with pTRzwf07, a low‐copy‐number plasmid that carries the same inducible construction as pTRzwf04, and with the pTEXP‐MMRPI vector that carries a TrpLE‐proinsulin hybrid gene. In this system, production of TrpLE‐proinsulin strongly reduces growth rate; however, overexpression of zwf gene recovers with a growth rate from 0.1 h−1 in the TrpLE‐proinsulin induced strain, to 0.37 h−1 when both zwf and TrpLE‐proinsulin genes were induced. In this paper, we show that the engineering of the pentose phosphate pathway by modulation of the zwf gene expression level partially overcomes the possible bottleneck for the supply of building blocks and reducing power synthesized through the PP pathway, that are required for plasmid replication and plasmid‐encoded protein expression. © 2004 Wiley Periodicals, Inc.
Tumor necrosis factor-alpha expression in ischemic neurons.

BACKGROUND AND PURPOSE Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with diverse proinflammatory actions, including endothelial leukocyte adhesion molecule expression. Since leukocytes infiltrate into ischemic brain lesions, the present study was conducted to examine whether TNF-alpha messenger RNA (mRNA) and peptide are expressed in the brain after experimental focal stroke and before leukocyte accumulation. METHODS TNF-alpha mRNA and protein expression were monitored in the ischemic and nonischemic cerebral cortex of rats after focal ischemia produced by permanent middle cerebral artery occlusion. The effect of TNF-alpha administered by microinjection into the brain cortex on leukocyte adherence to brain capillaries was also studied. RESULTS Induction of TNF-alpha mRNA, normalized to a standard reference rat macrophage TNF-alpha mRNA, was detected as early as 1 hour after middle cerebral artery occlusion. TNF-alpha mRNA was elevated by 3 hours (29 +/- 6% versus 2 +/- 1% in sham-operated rats) only in the ischemic cortex, with peak expression at 12 hours (104 +/- 8%; P < .01). Five days after middle cerebral artery occlusion, TNF-alpha mRNA levels in ischemic cortex were still significantly elevated (38 +/- 5%; P < .05). Also, TNF-alpha mRNA expression was greater in the ischemic cortex of spontaneously hypertensive rats than in normotensive rats (P < .05). Double-labeling, immunohistochemical studies revealed the presence of TNF-alpha protein localized within nerve fibers in the evolving infarct at 6 and 12 hours after ischemia and further expression in the tissues immediately adjacent to the infarct 24 hours after ischemia. After 5 days, the neuronally localized peptide had diminished greatly, but macrophages located within the infarcted tissues were immunoreactive. Cortical microinjections of TNF-alpha (10 ng in 1 microL) produced a significant neutrophil adherence/accumulation in capillaries and small blood vessels 24 hours later. CONCLUSIONS These results represent the first demonstration that focal cerebral ischemia in rats results in elevated TNF-alpha mRNA and protein in ischemic neurons. The neuronal expression of peptide appears to facilitate the infiltration of inflammatory cells that can further exacerbate tissue damage in cerebral ischemia and might contribute to increased sensitivity and risk in focal stroke.
REV I EW Ecological speciation

Howard D. Rundle* and Patrik Nosil Department of Zoology and Entomology, University of Queensland, Brisbane, Queensland 4072, Australia Department of Biological Sciences, Simon Fraser University, Burnaby, BC V5A 1S6, Canada *Correspondence: E-mail: h.rundle@uq.edu. au Abstract Ecological processes are central to the formation of new species when barriers to gene flow (reproductive isolation) evolve between populations as a result of ecologically-based divergent selection. Although laboratory and field studies provide evidence that ecological speciation can occur, our understanding of the details of the process is incomplete. Here we review ecological speciation by considering its constituent components: an ecological source of divergent selection, a form of reproductive isolation, and a genetic mechanism linking the two. Sources of divergent selection include differences in environment or niche, certain forms of sexual selection, and the ecological interaction of populations. We explore the evidence for the contribution of each to ecological speciation. Forms of reproductive isolation are diverse and we discuss the likelihood that each may be involved in ecological speciation. Divergent selection on genes affecting ecological traits can be transmitted directly (via pleiotropy) or indirectly (via linkage disequilibrium) to genes causing reproductive isolation and we explore the consequences of both. Along with these components, we also discuss the geography and the genetic basis of ecological speciation. Throughout, we provide examples from nature, critically evaluate their quality, and highlight areas where more work is required.
Neonatal Undernutrition and Amygdaloid Nuclear Complex Development: An Experimental Study in the Rat

This study describes the morphology of neurons from the basolateral (ABL), central (ACE), and medial (AM) nuclei of the amygdaloid complex in neonatally undernourished (U) and control (C) Wistar strain rats. The cells were impregnated with the Golgi-Cox technique and studied at the ages of 12, 20, and 40 days postnatally. In the U-pups the neurons of the three nuclei displayed a reduced somatic area compared to that of the C-group on Days 12 and 20. However, at 40 days, this difference diminished due to a reduction in the somatic area of the C-group. The dendritic area also appeared reduced on Days 12 and 20 in the U-group, but on Day 40 it reached control values. The neurons from ABL and ACE suffered a significant decrease in the number of dendritic branches due to undernutrition, but the AM nucleus did not show this change. The data suggest different vulnerability of these amygdaloid nuclei to neonatal undernutrition. The findings also suggest that the abnormal emotional response characteristic of perinatal undernourished rats could have a morphological cause.
The Influence of Mood on Attribution

Four studies show that mood systematically affects attributions of observed behavior by altering relative attention to actor and context. When the actor is more salient, sad people are more inclined to perceive an actor in stable trait terms and favor dispositional over situational explanations, whereas the opposite is true for happy people (Studies 1-3). However, when the context is made more salient, this pattern reverses, such that those in a negative mood make more situational attributions than those in a positive mood (Study 4). Taken together, these findings provide strong support for our hypothesis that mood and salience interact to affect attributions.
Translocation of rubella virus glycoprotein E1 into the endoplasmic reticulum

Rubella virus (RV) contains four structural proteins, C (capsid), E2a, E2b, and E1, which are derived from posttranslational processing of a single polyprotein precursor, p110. C protein is nonglycosylated and is thought to interact with RV RNA to form a nucleocapsid. E1 and E2 are membrane glycoproteins that form the spike complexes located on the virion exterior. Two different E1 cDNAs were used to analyze the requirements for translocation of E1 into the endoplasmic reticulum. Analysis of expression of these cDNAs both in vivo and in vitro showed that RV E1 was stably expressed and glycosylated in COS cells and correctly targeted into microsomes in the absence of E2 glycoprotein. The results provide experimental evidence that translocation of RV E1 glycoprotein into the endoplasmic reticulum is mediated by a signal peptide contained within the 69 carboxyl-terminal residues of E2.
Management of hyperlactatemia: no need for routine lactate measurements.

Despite the impressively bene®cial effects of antiretroviral medication for HIV-infected patients, it has become increasingly evident that prolonged therapy can also have adverse effects. One of the most fearful is the development of severe lactic acidosis, induced by the mitochondrial toxicity of nucleoside analogue reverse transcriptase inhibitors (NRTIs) [1]. Although initially believed to be an extremely rare event [2], recent studies demonstrated elevated serum lactate levels in asymptomatic patients receiving NRTIs [3±5], with an estimated incidence of between 15 and 35%. Without longitudinal studies it is not known whether severe NRTI-induced lactic acidosis (serum lactate level greater than 5 mmol/l, with a serum bicarbonate level lower than 20 mmol/l) is preceded by periods of mild hyperlactatemia (serum lactate levels between 2 and 5 mmol/l). It is possible that both represent the extremes of a single syndrome, because recent reports have appeared on patients with mild hyperlactatemia with symptoms similar to those of patients with lactic acidosis, including extreme fatigue, vomiting and abdominal pain [6,7].
Silent Scaffolds

Background: JNK kinases play an important role in cell death and differentiation. Results: Arrestin-3 mutant that binds ASK1, MKK4, and JNK3 normally without promoting JNK3 activation suppresses JNK3 activation in the cell. Conclusion: Modified scaffolding proteins can be used to regulate MAP kinase activity in vivo. Significance: Silent scaffolds are a novel type of molecular tool for manipulation of MAP kinase activity in cells. We established a new in vivo arrestin-3-JNK3 interaction assay based on bioluminescence resonance energy transfer (BRET) between JNK3-luciferase and Venus-arrestins. We tested the ability of WT arrestin-3 and its 3A mutant that readily binds β2-adrenergic receptors as well as two mutants impaired in receptor binding, Δ7 and KNC, to directly bind JNK3 and to promote JNK3 phosphorylation in cells. Both receptor binding-deficient mutants interact with JNK3 significantly better than WT and 3A arrestin-3. WT arrestin-3 and Δ7 mutant robustly promoted JNK3 activation, whereas 3A and KNC mutants did not. Thus, receptor binding, JNK3 interaction, and JNK3 activation are three distinct arrestin functions. We found that the KNC mutant, which tightly binds ASK1, MKK4, and JNK3 without facilitating JNK3 phosphorylation, has a dominant-negative effect, competitively decreasing JNK activation by WT arrestin-3. Thus, KNC is a silent scaffold, a novel type of molecular tool for the suppression of MAPK signaling in living cells.
Perinatal outcomes in gestational diabetes: a comparison of criteria for diagnosis.

OBJECTIVE The purpose of this study was to compare the perinatal outcomes of women after diagnosis of gestational diabetes by the current American College of Obstetricians and Gynecologists-National Diabetes Data Group recommendations with outcomes after diagnosis by the American Diabetes Association criteria. STUDY DESIGN We identified records of 242 women who had had the standard 3-hour oral glucose tolerance test between 1995 and 1999 at the Regional Medical center in Memphis. Patients were categorized into 1 of 3 groups as follows: euglycemic control subjects (n = 69), subjects with gestational diabetes diagnosed by the National Diabetes Data Group criteria (n = 130), and subjects with gestational diabetes diagnosed by the American Diabetes Association criteria (n = 43). Maternal and infant charts were reviewed. Primary outcomes included frequency of cesarean delivery, preeclampsia, and macrosomia. In univariate analysis the chi2 test was used to compare group differences, and in multivariate analysis we used stepwise logistic regression and controlled for confounding factors. RESULTS No differences existed among the 3 groups regarding maternal race, body mass index, history of preeclampsia, or family history of diabetes. The frequency of overall cesarean delivery, of cesarean delivery for macrosomia or arrest disorder, of preeclampsia, and of macrosomia did not differ significantly among the 3 groups. Neonatal hypoglycemia was more frequent in the groups with a diagnosis by the American Diabetes Association criteria (23.3%) and by the National Diabetes Data Group criteria (16.2%) than in the control subjects (7.2%), reaching near significance (P =.057). In the multivariate analysis, cesarean delivery for macrosomia or an arrest disorder correlated negatively with parity and positively with body mass index. Preeclampsia was associated with African American race and body mass index; macrosomia correlated with a history of macrosomia and familial diabetes. Neonatal hypoglycemia was more common in the American Diabetes Association group (odds ratio, 2.45; 95% confidence interval, 1.004-5.97) and in the insulin-requiring National Diabetes Data Group category (odds ratio, 3.71; 95% confidence interval, 1.20-11.44). CONCLUSION The benefits of defining an additional high-risk population of women with gestational diabetes by the American Diabetes Association criteria are unclear. Further large-scale prospective clinical trials are required.
Pediatric Feeding Disorders: Effectiveness of Multidisciplinary Inpatient Treatment of Gastrostomy-Tube Dependent Children

Effectiveness of multidisciplinary inpatient treatment of feeding-disordered children was sought through retrospective chart review of 40 gastrostomy-tube (i.e., G-tube) dependent children, ages 22 months to 7 years, with co-occurring medical conditions. Treatment effect analyzed from pre- and posttreatment measures of oral and G-tube caloric intakes resulted in a significant difference from admission to discharge for both oral intake, t(39) = 5.76, p < . 001 (d = 1.02); and G-tube dependency, t(39) = 10.94, p < . 001 (d = 2.03), with both showing strong treatment effects. Results indicated a highly reliable and valid method of treating severe pediatric feeding disorders.
Regulation of Emotion and Behavior Among 3- and 5-Year-Olds

In this cross-sectional study, the authors examined the relationship between emotion and behavior regulation in 3- and 5-year olds. Eighty-seven children performed a compliance sorting task. The authors manipulated the demand for emotion regulation by presenting and then hiding toys (low) or making toys visible (high). Mothers and teachers rated children's coping responses. Five-year-olds sorted less in the high condition than in the low condition, and 3-year-olds spent equal time sorting in both conditions. Compliance was positively correlated with problem-focused coping and negatively correlated with emotion-focused coping. Correlations between emotion and behavior regulation were stronger for the 5-year-olds. Age groups were differently affected by the higher demands of emotion regulation, indicating that the child's resources for regulation interact with the task demands to determine behavioral outcome.