Miracle-dz/UniFAR-FTUs huggingface dataset:
Sturkie's Avian Physiology

We all have our core trove of reference books that sit within arm’s reach. The good ones are binder-worn, and more than often, our students or lab mates have borrowed them and we have to track them down. How often do we turn to a reference book for a key bit of information instead of diving into the morass of online searching? If you’re like me, you probably can beat your new student every time in finding a key piece of information or key words from your tried and true reference books as they set off on a long journey of database searches. Unlike our predecessors, our libraries of reference texts cover broader fields of inquiry and are more numerous. New discovery is at the interface of disciplinary subjects and our bound library must increasingly reflect our attempts to be a polymath. Often our mostused reference books are not our subject of expertise, but the subject we never took a class in, and new editions rarely replace the old editions, they just update topics, dropping key pieces of information that should always remain at our finger tips. When it comes to the study of avian species and their biology and pathology, we all have our core reference books on nutrition, genetics, disease, reproduction, physiology, anatomy, and perhaps specialized areas such as welfare and management. The more comparative the text, often the more useful, and the index, tables, and figures are quintessential as we increase our expertise in that new field of inquiry or get last minute tidbits for a lecture. One of the bibles for avian biology that sits on my shelf, or is always floating around my lab, is Sturkie’s Avian Physiology, originally edited by Paul Sturkie. I keep the older and newest editions, and they are core to my research, teaching, and outreach as a university professor. Not knowing if my custom of using hard copies of references books like Sturkie’s Avian Physiology was dated or trending, I polled some of my colleagues across multiple disciplines (mine is nutrition and immunology) to see if they had heard of or used Sturkie’s Avian Physiology, 6th edition (or prior) edited by Professor Colin G. Scanes in 2015. I polled only a handful of colleagues in the areas of poultry science, avian diseases, wildlife ecology, and wildlife diseases. An interesting pattern emerged. My wildlife/disease colleagues, unless they specifically worked in the area of physiology, generally were not aware of the reference text. Those who specifically taught or researched wildlife physiology praised the text. K. C. Klasing, professor of avian biology at UC Davis, an instructor of avian physiology, and author of Comparative Avian Nutrition replied:
A better statistical method of predicting postsurgery soft tissue response in Class II patients.

OBJECTIVE To propose a better statistical method of predicting postsurgery soft tissue response in Class II patients. MATERIALS AND METHODS The subjects comprise 80 patients who had undergone surgical correction of severe Class II malocclusions. Using 228 predictor and 64 soft tissue response variables, we applied two multivariate methods of forming prediction equations, the conventional ordinary least squares (OLS) method and the partial least squares (PLS) method. After fitting the equation, the bias and a mean absolute prediction error were calculated. To evaluate the predictive performance of the prediction equations, a leave-one-out cross-validation method was used. RESULTS The multivariate PLS method provided a significantly more accurate prediction than the conventional OLS method. CONCLUSION The multivariate PLS method was more satisfactory than the OLS method in accurately predicting the soft tissue profile change after surgical correction of severe Class II malocclusions.
Acute Remapping within the Motor System Induced by Low-Frequency Repetitive Transcranial Magnetic Stimulation

Repetitive transcranial magnetic stimulation (rTMS) of human primary motor cortex (M1) changes cortical excitability at the site of stimulation and at distant sites without affecting simple motor performance. The aim of this study was to explore how rTMS changes regional excitability and how the motor system compensates for these changes. Using functional brain imaging, activation was mapped at rest and during freely selected finger movements after 30 min of 1 Hz rTMS. rTMS increased synaptic activity in the stimulated left M1 and induced widespread changes in activity throughout areas engaged by the task. In particular, movement-related activity in the premotor cortex of the nonstimulated hemisphere increased after 1 Hz rTMS. Analyses of effective connectivity confirmed that the stimulated part of M1 became less responsive to input from premotor and mesial motor areas. Conversely, after rTMS our results were consistent with increased coupling between an inferomedial portion of left M1 and anterior motor areas. These results are important for three reasons. First, they show changes in motor excitability to central inputs from other cortical areas (as opposed to peripheral or exogenous inputs used in previous studies). Second, they suggest that maintenance of task performance may involve activation of premotor areas contralateral to the site of rTMS, similar to that seen in stroke patients. Third, changes in motor activations at the site of rTMS suggest an rTMS-induced remodeling of motor representations during movement. This remapping may provide a neural substrate for acute compensatory plasticity of the motor system in response to focal lesions such as stroke.
Molecular Cloning and Sequencing of a Novel Invertebrate Intestinal Mucin cDNA*

The first invertebrate intestinal mucin, termed insect intestinal mucin (IIM), was recently identified fromTrichoplusia ni larvae (Wang, P., and Granados, R. R. (1997) Proc. Natl. Acad. Sci. U. S. A. , in press). We report the cDNA cloning and sequencing of IIM, which is only the second completely sequenced intestinal mucin after human intestinal mucin, MUC2. To clone and sequence the cDNA for IIM, a T. ni larval midgut cDNA expression library was constructed and screened with an anti-IIM antiserum. Two full-length cDNA clones for IIM were identified and sequenced. The deduced proteins from the two cDNA clones contained 807 and 788 amino acid residues, respectively. The structural organization of IIM is similar to that of MUC2, containing a 25-amino acid signal leading sequence and two threonine/proline/alanine-rich tandem repeat domains flanked by cysteine-rich sequences. One tandem repeat domain contained two repeating units, TTTQAP and AATTP, and the other contained one repeating unit, TAAP. The cysteine-rich regions showed potential chitin binding features. By immunolocalization in tissue sections, it was determined that IIM is expressed in midgut tissues. The IIM mRNA is abundant in the midgut tissue, and Northern blot analysis indicated that IIM transcripts were not polydispersed as is found in mammalian mucin transcription.
Evidence that Increased Acetaminophen use in Genetically Vulnerable Children Appears to be a Major Cause of the Epidemics of Autism, Attention Deficit with Hyperactivity, and Asthma

It appears that the marked increase in the rate of autism, asthma, and attention deficit with hyperactivity throughout much of the world may be largely caused by the marked increase in the use of acetaminophen in genetically and/or metabolically susceptible children, and the use of acetaminophen by pregnant women. Toxicity of acetaminophen may cause autism by overloading the defective sulfation pathway catalyzed by phenolsulfotransferase, which is deficient in autism, leading to overproduction of the toxic metabolite N -acetylp-benzoquinone imine (NAPQI). Increased levels of NAPQI reduce the ability to detoxify a host of toxic chemicals in the environment, increasing oxidative stress, which leads to protein, lipid, and nucleic acid damage from free radicals. Epidemiological evidence also supports the association of increased acetaminophen usage with autism, DVWKPD, and attention deficit with hyperactivity. The marked increases in the incidences of autism, asthma, and attention deficit disorder in the United States coincide with the replacement of aspirin by acetaminophen in the 1980s. The characteristic loss of Purkinje cells in the brains of people with autism is consistent with depletion of brain glutathione due to excess acetaminophen usage, which leads to premature brain Purkinje cell death. The anomalous hair mercury concentrations of children with autism are consistent with exposure of growing hair proteins to NAPQI derived from acetaminophen, which competitively inhibits the reaction of mercury with hair sulfhydryl groups. Finally, large-scale faulty production of acetaminophen products, such that the labeled values were exceeded by the true concentrations, in addition to contamination with bacteria and tribromoanisole, may have greatly increased the chances of children receiving overdosages of acetaminophen and potential toxins for perhaps as long as a decade.
High Incidence of Invasive Group B Streptococcal Infections in HIV-Exposed Uninfected Infants

OBJECTIVES: The occurrence of an unusual number of group B streptococcal (GBS) infections in HIV-exposed uninfected (HEU) infants who were followed in our center prompted this study. The objective of this study was to describe and compare the incidence and clinical presentation of GBS infections in infants who were born to HIV-infected and -uninfected mothers. METHODS: All cases of invasive GBS infections in infants who were born between 2001 and 2008 were identified from the database of HEU infants and from the microbiology laboratory records. The medical charts of all infants with GBS infection were reviewed. RESULTS: GBS invasive infections were described for 5 (1.55%) infants who were born to 322 HIV-infected mothers who delivered in our center. The incidence of GBS infections during the same period was 16 (0.08%) of 20 158 infants who were born to HIV-uninfected mothers. One HEU infant presented a recurrent infection 28 days after completion of treatment for the first episode. Late-onset infection was more frequent in HEU infants (5 of 6 vs 2 of 16 episodes in the control population). The diseases were also more severe in HEU infants with 5 of 6 sepsis or sepsis shock in HEU infants versus 10 of 16 in control subjects, and most HEU infants had leukopenia at onset of infection. CONCLUSIONS: The incidence of GBS infection was significantly higher in HEU infants than in infants who were born to HIV-uninfected mothers. These episodes of GBS sepsis in HEU infants were mostly of late onset and more severe than in the control population, suggesting an increased susceptibility of HEU infants to GBS infection.
Procalcitonin and cytokine levels: Relationship to organ failure and mortality in pediatric septic shock

Background Procalcitonin (PCT), a marker of bacterial sepsis, may also act as a mediator of the inflammatory response to infection, and thus influence outcome. Objective To investigate the relationship between PCT, interleukin (IL)-10, tumor necrosis factor (TNF), organ failure, and mortality in pediatric septic shock. Design Prospective observational study. Setting A 16-bed pediatric intensive care unit of a university hospital. Patients A total of 75 children with septic shock having a median age of 43.1 months (range, 0.1–192 months). Children who had received antibiotics for >24 hrs were excluded. A total of 37 patients (49%) had meningococcal disease, and 72 patients (96%) required mechanical ventilation. Interventions The pediatric risk of mortality (PRISM) score, multiple organ system failure (MOSF) score, duration of ventilation, length of ICU stay, and outcome were recorded. PCT, IL-10, and TNF were measured at admission to the intensive care unit. Sequential PCT levels were available at 0 hrs and 24 hrs in 39 patients (52%). Results Observed mortality was 21/75 (28%). Data are median (range). The admission PCT (p = .0002) and TNF levels (p = .0001) were higher in children with higher MOSF scores. In survivors and nonsurvivors, the admission PCT was 82 ng/mL vs. 273 ng/mL (p = .03), IL-10 was 62 pg/mL vs. 534 pg/mL (p = .03), and TNF was 76 pg/mL vs. 480 pg/mL (p = .001), respectively. Area under the mortality receiver operating characteristic curve was 0.73 for PCT, 0.67 for IL-10, and 0.76 for TNF, compared with 0.83 for the PRISM score. Of 39 children, 16 (41%) with sequential PCT measurements showed no fall in PCT after 24 hrs treatment. These children had higher admission levels of IL-10 (p = .03), and TNF (p = .03) compared with children who demonstrated a subsequent fall in PCT. Although the former did not have a higher median PRISM (p = .28) or MOSF score (p = .19), observed mortality was 44% (7 of 16) compared with 9% (2 of 23) (p = .02). Conclusion The admission PCT, like TNF and IL-10, is related to the severity of organ failure and mortality in children with septic shock. A fall in PCT after 24 hrs of treatment may have favorable prognostic significance.
A Min–Max Model Predictive Control Approach to Robust Power Management in Ambulatory Wireless Sensor Networks

This paper addresses the problem of transmission power control within a network of resource-constrained wireless sensors that operate within a particular ambient healthcare environment. Sensor data transmitted to a remote base station within the network arrive subject to node location, orientation, and movement. Power is optimally allocated to all channels using a novel resource efficient algorithm. The proposed algorithm is based on a computationally efficient min-max model predictive controller that uses an uncertain linear state-space model of the tracking error that is estimated via local received signal strength feedback. An explicit solution for the power controller is computed offline using a multiparametric quadratic solver. It is shown that the proposed design leads to a robust control law that can be implemented quite readily on a commercial sensor node platform where computational and memory resources are extremely limited. The design is validated using a fully IEEE 802.15. 4 compliant testbed using Tmote Sky sensor nodes mounted on fully autonomous MIABOT Pro miniature mobile robots. A repeatable representative selection of scaled ambulatory scenarios is presented that is quite typical of the data that will be generated in this space. The experimental results illustrate that the algorithm performs optimal power assignments, thereby ensuring a balance between energy consumption and a particular outage-based quality of service requirement while robustly compensating for disturbance uncertainties such as channel fading, interference, quantization error, noise, and nonlinear effects.
SesI May Be Associated with the Invasiveness of Staphylococcus epidermidis

Staphylococcus epidermidis is a commensal bacterium which widely colonizes in human skin and mucous membrane and rarely causes clinically manifested infections. S. epidermidis surface protein I (SesI) is considered to be the major virulence factor of S. epidermidis infection, but its pathogenesis is not clear. Here, we demonstrated that the prevalence of sesI among S. epidermidis invasive isolates (20.8%, 26/125) was significantly higher than that among colonizing isolates (3.8%, 4/106). The positive rates of biofilm-associated genes (aap, icaA, IS256) and resistance-associated genes mupA among the sesI-positive isolates were significantly higher than those among sesI-negative isolates (p < 0.05). And antimicrobial susceptibility testing showed that the resistance rates of sesI-positive isolates to ciprofloxacin, gentamicin and trimethoprim/sulfamethoxazole were significantly higher than those among sesI-negative isolates. Interestingly, 80.8% (21/26) of sesI-positive isolates belong to ST2 determined by MLST, while ST2 was not found among any of the 99 sesI-negative invasive isolates, indicating that there is a strong association between carriage of sesI and ST2 clone. In order to further study the role of sesI gene in pathogenesis, the sesI gene mutant (S. epidermidis RP62AΔsesI) and complementary expression strain (S. epidermidis RP62AΔsesI-C) were successfully constructed. All experimental data indicated that sesI may promote S. epidermidis to adhere and aggregate, but it had no obvious effect on the mature stage of biofilm formation. Taken together, these results suggest that sesI, along with antimicrobial and other biofilm-associated genes enables S. epidermidis easier for colonization and adhesion and contributes to the spread of S. epidermidis, especially ST2 clone.
Forecasting Bull and Bear Markets: Evidence from China

ABSTRACT This article extends previous empirical research to forecast Chinese bull and bear stock markets by using three types of binary probit time series models, which are static, autoregressive, and dynamic autoregressive models. This study shows that the dynamic auto regressive model performs the best both in- and out-of-sample. The inflation and market return variables significantly affect the market forecast. The dynamic autoregressive model has successfully forecast the bull and bear markets since 2007. The investment strategy based on this model performs better than the simple buy-and-hold strategy, especially after the Chinese government reformed the non-tradable shares in 2005.
Blockade of the T cell immunoglobulin and mucin domain protein 3 pathway exacerbates sepsis‐induced immune deviation and immunosuppression

Sepsis is a life‐threatening condition, but the pathophysiological basis and biomarkers for the monitoring of sepsis and as targets for therapy remain to be determined. We have shown previously that T cell immunoglobulin and mucin domain protein 3 (Tim‐3), a negative immune regulator, is involved in the physiopathology of sepsis, but the underlying mechanisms remain unclear. In the present study, we showed that Tim‐3 signalling modulated the response patterns of both macrophages and T helper cells in sepsis. Blockade of the Tim‐3 pathway exacerbated sepsis‐induced proinflammatory macrophage responses and lymphocyte apoptosis during the early phase of sepsis, and enhanced the shift to anti‐inflammatory responses for both macrophages and T helper cells during the late phase of sepsis. Tim‐3 signalling was found to regulate CD80 and CD86 expression on macrophages both in vivo and in vitro. Co‐culture of T cells with Tim‐3 knock‐down macrophages led to a biased T helper type 2 (Th2) response, partially explaining how Tim‐3 signalling shapes inflammation patterns in vivo. Further studies on this pathway might shed new light on the pathogenesis of sepsis and suggest new approaches for intervention.
Influence of Alkyl Chain Length of Benzalkonium Chloride on Acute Corneal Epithelial Toxicity

Purpose: To evaluate acute corneal epithelial toxicity induced by benzalkonium chloride (BAC) homologs with different alkyl chain lengths using an in vivo electrophysiological method. Methods: BAC homologs with C12, C14, and C16 alkyl chain lengths were used at concentrations of 0.0025%, 0.005%, and 0.01%, respectively. Cytotoxicity of BAC homologs on the normal rabbit corneal epithelial cells was examined by using a WST-1 assay. Corneal transepithelial electrical resistance (TER) was measured in living Japanese white rabbits by 2 Ag/AgCl electrodes placed in the anterior aqueous chamber and on the cornea. TER changes were then evaluated after a 60-second exposure to these BAC homologs. Morphological changes in corneal epithelium after exposure to the BAC homologs were examined using scanning electron microscopy. The antimicrobial activity of BAC homologs against Escherichia coli was also assessed. Results: All BAC homologs caused cytotoxicity and corneal barrier dysfunction in a concentration-dependent manner. However, the degree of corneal toxicity differed among the BAC homologs. Based on cytotoxicity and TER measurement, C14-BAC caused the greatest corneal impairment followed in order of severity by mixed BAC/C16-BAC and C12-BAC. Scanning electron microscopy images indicated an intact corneal epithelium after exposure to 0.005% C12-BAC, whereas 0.005% C14-BAC damaged the epithelium. There were no remarkable differences noted in the antimicrobial activity among the BAC homologs. Conclusions: Acute corneal epithelial toxicity induced by BAC homologs depends on the alkyl chain length. Thus, the use of C12-BAC instead of commercially available BAC is potentially safer for patients undergoing ophthalmological pharmacotherapy.
Wide gene expression profiling of ischemia‐reperfusion injury in human liver transplantation

Ischemia‐reperfusion injury (IRI) causes up to 10% of early liver failures in humans and can lead to a higher incidence of acute and chronic rejection. So far, very few studies have investigated wide gene expression profiles associated with the IRI process. The discovery of novel genes activated by IRI might lead to the identification of potential target genes for the prevention or treatment of the injury. In our study, we compared gene expression levels in reperfused livers (RL group) vs. the basal values before retrieval from the donor (basal liver [BL] group) using oligonucleotide array technology. We examined 10 biopsies from 5 livers, analyzing approximately 33,000 genes represented on the Affymetrix HG‐U133APlus 2.0 oligonucleotide arrays (Affymetrix, Santa Clara, CA). About 13,000 individual genes were considered expressed in at least 1 condition. A total of 795 genes whose expression is significantly modified by ischemia‐reperfusion in human liver transplantation were identified in this study. Some of them are likely to be completely activated by IRI, as they are not expressed in basal livers. The supervised gene expression analysis revealed that at least 12% of the genes involved in the apoptotic process, 12.5% of the genes involved in inflammatory processes, and 22.5% of the genes encoding for heat shock proteins are differentially expressed in RL samples vs. BL samples. Furthermore, IRI induces the upregulation of some genes' coding for adhesion molecules and integrins. In conclusion, we have identified a relevant amount of early genes regulated in the human liver after 7–9 hours of cold ischemia and 2 hours from reperfusion, many of them not having been described before in this process. Their analyses may help us to better understand the pathophysiology of IRI and to characterize potential target genes for the prevention or treatment of the liver injury in order to increase the number of patients that successfully undergo transplantation. Liver Transpl 13:99–113, 2007. © 2006 AASLD.
Automatic formatted transcripts for videos

Multimedia content may be supplemented with time-aligned closed captions for accessibility. Often these captions are created manually by professional editors — an expensive and timeconsuming process. In this paper, we present a novel approach to automatic creation of a well-formatted, readable transcript for a video from closed captions or ASR output. Our approach uses acoustic and lexical features extracted from the video and the raw transcription/caption files. We compare our approach with two standard baselines: a) silence segmented transcripts and b) text-only segmented transcripts. We show that our approach outperforms both these baselines based on subjective and objective metrics.