Background: Postpartum hemorrhage was a deadly characteristic eliminated by evolution. No animals hemorrhage. The first case of documented human postpartum hemorrhage appears in the literature around 1400 AD. Human PPH appears to be a relatively recent occurrence, perhaps coinciding with the decrease in the use of squatting. A protocol called Judy’s 3,4,5 calls for squatting delivery of the placenta between 3 and 5 minutes postpartum. Methodology: A retrospective cohort study of 1,024 planned, attended homebirths in Israel using Judy’s 3,4,5 minute third stage protocol compared to 2,691 planned homebirths resulting in vaginal births in British Columbia using active management or expectant management of the third stage of labor. Results: Among similar groups of low risk births, active management, or expectant management resulted in 4.1% PPH over 500 cc, whereas Judy’s 3,4,5 minute protocol resulted in 0% PPH over 500 cc. Conclusion: Judy’s 3,4,5 minute protocol continues to result in less blood loss than any other third stage protocol at vaginal birth. The average blood loss is 100 cc for the first two hours after the birth of the newborn.

We introduce a straightforward method for the preparation of novel starch-based ultramicroporous carbons (SCs) that demonstrate high CH4 uptake and excellent CH4/N2 selectivity. These SCs are derived from a combination of starch and 1-6 wt. % of acrylic acid, and the resulting materials are amenable to surface cation exchangeability as demonstrated by the formation of highly dispersed K+ in carbon precursors. Following activation, these SCs contain ultramicropores with narrow pore-size distributions of <0.7 nm, leading to porous carbon-rich materials that exhibit CH4 uptake values as high as 1.86 mmol/g at 100 kPa and 298 K, the highest uptake value for CH4 to date, with the IAST-predicted CH4/N2 selectivity up to 5.7. Both the potential mechanism for the formation of narrow pores and the origin of the favorable CH4 adsorption properties are discussed and examined. This work may potentially guide future designs for carbon-rich materials with excellent gas adsorption properties.

From the date of unravelling the sequence of pandemic phenomena causing novel coronavirus (named SARS-CoV-2/COVID-19), there have been limited but key molecular and structural advancements made a great impact in COVID 19 research and in the development of therapeutics in a right direction. The solving the structure of SARS-CoV-2 spike glycoprotein and its interactions with ACE2/CD26 are the two major findings were proposing the possible mode of SARS-CoV-2 entry into the host cell. Following unravelling the camouflaging glycan shied novel incorporation of Furin cleavage site underlines the district features of a novel coronavirus from the previous. Taking these key molecular and structural advancements, we developed the structural model of the SARS-CoV-2 interacting with human host proteins for adhesion and virulence for easy and scientific understanding for the general reader.

Background and Purpose: The aim of this study was to investigate the mechanism of a possible differential effect of Neocuproine (NC), selective Cu(1) chelator, in rat and mouse bladder tissues. Experimental Approach: Bladder function was evaluated by 1. in vitro isolated bladder strips, 2. in vitro preparations of whole bladders and 3. İn vivo cystometrogram (CMG) in rat and mouse. Selective Cu(I) and Cu(II) chelators and non-selective purinergic antagonists were examined on EFS-induced bladder contractions in isolated bladder strips. The spontaneous contraction activities of whole bladders were recorded to evaluate the amplitudes and frequencies. In CMGs experiments, the values of maximum bladder pressure during micturition and intercontraction intervals (ICI) were evaluated. Key Results: Whereas Neocuproine (NC) enhances the opposite effect on isolated bladder strips and whole bladder experiments, this opposite effect was not observed in in vivo CMG experiments in rat and mouse. NC caused a significant suppression on spontaneous contractions and baseline tonus in isolated mouse bladder tissues, whereas it caused facilitating effects in the rat. However, NC significantly decreased the ICI in both rat and mouse in CMGs. Conclusion and Implications: The effect of Neocuproine on rat and mouse bladder activity is likely to be the role of myogenic mechanisms. It is possible to trigger mechanisms associated with intracellular calcium (Ca2+) reduction and purinergic pathway, P2X purinoceptors besides P2Y purinoceptors, may have an important role in the inhibitory activity of NC on mouse bladder.

When establishing a hypothesis testing procedure to ensure its credibility, the most significant step is unquestionably to select and/or compute the optimal type-I and type-II error probabilities, namely the producer’s and consumer’s risks, or α & β errors, respectively if the research hypothesis is set to be a good product vs bad. This article is fundamentally opposed to conventionally and judgmentally picking at best a subjective type-I error probability (α error) and it therefore outlines a game theoretic approach, i.e. that of von Neumann, to this historically century-old unresolved paradigm to justify optimal choices when relevant market-centric factors such as cost and utility are incorporated for input data. A game theory-based algorithmic methodology and several detailed numerical examples of practical nature with specific emphasis to company-specific acceptance sampling plans (including a simple hospital scenario) for quality control are studied. A side benefit of this method, in addition to improving the enterprise acceptance sampling plans, is to transform the traditional hypothesis testing procedure so as to make sound engineering decisions from a “subjective” to an “objective” stance, provided that the monetary cost and utility values as consequences to committing error and non-error combinations are available.

Abstract Ebola virus is one of the most deadly pathogens known to infect humans. The current Ebola outbreak in West Africa is unprecedented in magnitude and duration and, as of November 30, 2014, shows no signs of abating. For the first time, cases of Ebola virus disease have been diagnosed in the US, originating from patients who traveled during the incubation period. The outbreak has generated worldwide concern. It is clear that U.S. physicians need to be aware of this disease, know when to consider Ebola and how to care for the patient as well as protect themselves. Children comprise a small percentage of all cases globally, likely because of their lower risk of exposure given social and cultural practices. Limited evidence is available on pediatric disease course and prognosis. In this article, we present an overview of the pathogen, its epidemiology and transmission, clinical and laboratory manifestations, treatment and infection control procedures, with an emphasis on what is known about Ebola virus disease in the pediatric population. Ebola virus is one of the most virulent pathogens known to infect humans.1 The first recognized Ebola outbreak occurred in 1976, near the Ebola River in Zaire (now Democratic Republic of Congo, DRC). Over the past 40 years, more than 20 outbreaks have occurred in Africa, with most of the known outbreaks occurring in the past 20 years.2,3 Before the 2014 epidemic, over 2300 cases with greater than 1500 deaths had been documented from this disease.2 The current outbreak in West Africa has so far affected more people than all previous Ebola outbreaks combined4 : as of January 20, 2015, the cumulative number of probable, suspect and laboratory-confirmed cases attributed to Ebola virus was more than 21,000, with greater than 8500 deaths.5 These numbers likely represent underestimates of the outbreak's true size because of poor local health system infrastructure, with many patients being cared for outside hospital settings, or not reported.6 The unprecedented size and scale of this outbreak have generated worldwide concern, not only in part because it can destabilize the fragile social and economic milieu and healthcare systems of the involved countries, but also because it has raised fears of spread beyond the African continent. It has thus become a massive focus of international public health action.7 The first few cases of this disease have now occurred in the US. Given that this epidemic will likely last for at least several more months,8 additional patients with Ebola virus disease (EVD) may present to health care settings in the US. Therefore, an improved understanding of EVD among U.S. healthcare providers, especially infectious diseases specialists, is warranted. This article summarizes current knowledge on EVD, its epidemiology and clinical presentation as well as treatment and infection control procedures, with a focus on summarizing the limited available understanding of the effects of EVD in infants and children. EBOLA VIRUS: EPIDEMIOLOGICAL AND CLINICAL FEATURES Epidemiology The genus Ebolavirus is composed of single-stranded, enveloped, filamentous RNA viruses, that, together with the Marburgvirus genus, comprise the family Filoviridae.3,9 Ebola and Marburg viruses are antigenically distinct but cause similar illnesses.10 These viruses have classically been referred to as hemorrhagic fever viruses because of their clinical manifestations, which can include coagulation defects, capillary leak and shock; however, the disease caused by infection with viruses in the Ebolavirus genus is now referred to as EVD. There are currently 5 species in the Ebolavirus genus; Tai Forest ebolavirus, Sudan ebolavirus (SUDV), Zaire ebolavirus (Ebola virus, EBOV), Bundibugyo ebolavirus (Bundibugyo virus) and Reston ebolavirus (Reston virus, RESTV). These viruses differ in their virulence for humans. Tai Forest ebolavirus has only been clearly documented in one individual, and the case was not fatal. Mortality with SUDV (41–65%) and Bundibugyo virus (40%) is lower than the mortality seen with EBOV (57–88%). RESTV is named after Reston, Virginia, where it was first described in 1989 in cynomolgus macaques imported from the Philippines and has been reported to cause illness in primates but not in humans. Although serologic conversion was detected among scientists working with the infected monkeys, RESTV has not caused symptomatic disease in humans.1,3,9 Some studies of seroprevalence during EVD outbreaks have shown a small percentage (<2%) of the population having IgG antibodies to Zaire and SUDV, suggesting that subclinical infection may occur but is not common.11–13 With the exception of an outbreak of Marburg virus among vaccine manufacturing plant workers in Europe who came in contact with infected monkeys from Uganda in 1967,1 all filovirus human outbreaks before 2014 have occurred in Africa, with the frequency of recognized outbreaks increasing since 1990.3 EVD was first recognized in 1976, when 2 unrelated epidemics occurred in northern Zaire and southern Sudan; disease recurred in the same area of the Sudan in 1979, but EVD was not recognized again until 1994. The current outbreak, caused by EBOV, started in Guinea in late 2013, subsequently spread to Liberia, Sierra Leone, Nigeria, Senegal and Mali and continues unabated in the first 3 countries above.7,14 EBOV may have also been spreading among primates3,8 ; the great apes are likely dead-end hosts like humans. EVD is a zoonotic disease, but its natural animal reservoir remains unknown. Several species of small animals have been implicated as reservoirs; bats seem to be the most likely culprit based on epidemiologic evidence.15 Evidence that fruit bats are naturally infected by EBOV has been documented,16 but virus isolation has not been successful from bats or any other animal species to date. Sequence analysis of viruses indicates that the 2014 epidemic in West Africa has resulted from sustained person to person transmission, without additional introduction from animal reservoirs.3 Modes of Transmission The main routes of Ebola virus transmission are direct contact with a symptomatic Ebola patient's blood and body fluids (including but not limited to urine, feces, vomitus, saliva and sweat) through breaks in the skin or through inoculation into the mouth, nose or eyes.3 Human infection can also occur through contact with wild animals, such as by hunting, butchering or preparing meat from infected animals. Ritual washing of Ebola victims at funerals is a type of direct contact that plays an important role in Ebola transmission among humans.9 Transmission to household contacts is associated with close contact with sick patients, their body fluids or their remains.9 Unsafe medical procedures, such as injections employing reused syringes and improperly sterilized needles, have also played a role in some Ebola outbreaks; accidental needle stick injuries have led to isolated cases among laboratory personnel working in research laboratories.3,9 A nosocomial outbreak occurred in DRC in 1995 when a patient hospitalized with abdominal pain underwent an exploratory laparotomy; the entire surgical team became infected.17 Ebola virus spread from these workers to other hospital staff, patients and family members through direct physical contact. Healthcare workers are at risk for infection if they care for a patient with EVD without appropriate protective measures, and this has been a major route of transmission in some outbreaks.9 As of January 20, 2015, 828 health care workers are known to have become infected as a result of the current outbreak in West Africa, and 499 have died.18 The typical pattern of transmission of EVD to health care workers is from an infected patient to his or her primary caretaker while symptomatic, with subsequent spread from the caretaker to his or her primary caretaker. Household members who did not share nursing duties have remained unaffected, even if they slept in the same room. This pattern further suggests that transmission without direct contact with the patient is an unlikely route.17 Clinical Manifestations The incubation period is typically 8–10 days (range, 2–21 days, though it may be shorter when transmission has occurred through contaminated injection needles).19 Following the incubation period, there is usually an abrupt onset of fever, chills, malaise, anorexia, severe Kourtis et al. Page 3 Pediatr Infect Dis J. Author manuscript; available in PMC 2016 August 01. Author Manuscript Author Manuscript Author Manuscript Author Manuscript headache and myalgias of the trunk and lower back. Some patients may develop a diffuse maculopapular rash by days 5–7 of illness, mainly on the trunk. These initial symptoms are nonspecific and can easily be mistaken for other, endemic infectious diseases, such as malaria, typhoid fever, yellow fever or, particularly in the case of children, for other infections with exanthems, such as measles or meningococcemia. Gastrointestinal symptoms, including vomiting, nausea, watery diarrhea and abdominal pain, usually develop several days after the initial nonspecific presentation and become the predominant clinical feature. Bleeding is not universally present (less than 50% of patients)20,21 but can occur later in the course of the disease (usually around day 5–7), manifesting as petechia, bruising, oozing from venipuncture sites and/or mucosal hemorrhage. Conjunctival injection and dark red discoloration of the soft palate are common physical findings. Central nervous system involvement is often manifested by somnolence, delirium, seizures or coma.9 Pregnant women may experience spontaneous miscarriages, and they also seem to be at higher risk for severe illness and death.22 In addition to extensive tissue damage of some organs, filoviruses also induce a systemic inflammatory syndrome by causing the release of cytokines, chemokines and other proinflammatory mediators.23 In nonfatal cases, patients improve typically 6–11 days from onset of symptoms.10 Fatal disease is associated with more severe clinical signs early in infection, with progression to disseminated intravascular coagulation, septic shock and multiorgan failure. Death usually occurs between 6 and 16 days (mostly around the 9th day) after symptom onset.10 Laboratory findings in EVD patients include leukopenia, thrombocytopenia, electrolyte abnormalities, transaminase elevations and renal and coagulation abnormalities.9,10 Other findings include a marked decrease in albumin (reflective of a capillary leak syndrome) and elevated amylase levels. Patients with evidence of severe intravascular volume depletion, metabolic abnormalities, tachypnea, anuria, delirium, coma and shock have a poor prognosis.9,10 Elevated levels of several cytokines and chemokines are also associated with a worse clinical outcome.23,24 Convalescence is prolonged, marked by weakness, fatigue, arthralgia and failure to regain weight lost during the illness. Extensive skin sloughing and hair loss are also commonly observed, as are neuropsychiatric symptoms.3,10 Presence of thrombocytopenia and leukopenia with elevated transaminase levels is characteristic of filovirus disease as well as some other viral hemorrhagic fevers, but a severe progressive course with abdominal pain and diarrhea should lead to suspicion of a filovirus.Diagnosis and Care of the Infected Patient Laboratory diagnosis of Ebola virus infection can be made by detection of RNA or viral antigens in blood or other body fluids, using reverse transcription-polymerase chain reaction (RT-PCR), antigen capture enzyme immunoassay or virus isolation.9,10 These tests are generally performed only in specialized laboratories. Most acute infections are identified through RT-PCR; virus is generally detectable between 3 and 10 days from the onset of symptoms.25 In survivors, viremia usually resolves during the second week, in association with the appearance of virus-specific antibodies.9,10 However, virus can persist for weeks in particular body fluids, such as semen. Studies of survivors of the outbreak showed that viral RNA sequences could be detected in the semen for up to 91 days after disease onset26; studies from a 2000 Gulu, Uganda, outbreak showed that virus could be isolated from semen 82 days after disease onset.27,28 Patients typically seroconvert around days 8–12,9 but in fatal cases, antibodies are often not be detected before death.12 IgM antibodies detected by enzyme-linked immunosorbent assay may be detected in early convalescence,12 but IgG serologic testing may yield false-positive or irreproducible results.9 Gingival brushings may yield positive RT-PCR results during later stages of infection when gingival bleeding is common.10 Virus can be identified in postmortem tissue, such as skin, with immunohistochemical identification of antigen.10 There is currently no specific treatment for EVD. Supportive care with special attention to fluid and electrolyte management and maintenance of circulatory function is indicated.10,25 Analgesia and sedation may be useful to prevent agitation.10 Procedures and medications that increase the risk of bleeding should be considered weighing the potential benefits and risks to the patient. Replacement of coagulation factors and platelets may be necessary.9 Male patients who recover should be counseled regarding the risk of sexual transmission to partners for at least approximately 3 months after recovery, based on isolation of infectious virus from the semen of a survivor 82 days after disease onset and of viral sequences 91 days after symptom onset.27,28 Even though there are no approved therapies for patients with EVD, experimental therapies are in development. A cocktail of 3 monoclonal antibodies directed against the Ebola viral glycoprotein (ZMapp) prevented the death of Ebola-infected macaques, even when initiated after the animals had developed full clinical symptoms.29 This cocktail has been administered to 4 healthcare workers during the 2014 outbreak, 2 of whom survived and recovered.30,31 Controlled studies are needed to evaluate this and other novel treatments.32 A WHO expert panel33 has recommended considering the use of whole blood or serum from convalescent EVD survivors in the treatment of affected patients. Additionally, in the only human trial of convalescent serum, 7 of 8 patients who received the product survived, but these same 7 patients were in the second week of illness (and therefore more likely to recover regardless of intervention) and the 1 patient who died received the transfusion at day 4.34 Once data were adjusted for age, sex and the days since onset of symptoms, no statistical evidence of a survival benefit because of the receipt of blood transfusion was evident in this small sample.35 At this time, there are no approved forms of preexposure or post-exposure prophylaxis; however, several vaccine candidates are in development or about to be tested in clinical trials.36 Although guidelines on infection control procedures in the US are evolving, the most updated Centers for Disease Control and Prevention (CDC) guidance can be found on the CDC website.33 Soiled items and infectious secretions should be handled in a way that protects both healthcare personnel and the community.37,38 Environmental cleaning and disinfection with appropriate hospital disinfectants are needed.9,10,37 Heightened awareness in recognition of initial cases and institution of appropriate barrier nursing17,37 remain essential for the containment of outbreaks,9 as is strict isolation of cases.17,37,39.  Primary prevention measures are limited by the lack of knowledge of the natural reservoir. Community education that attempts to modify high-risk practices in African settings, for example, through altering traditional funeral practices and avoiding contact with bush meat, has been used during outbreaks. However, acceptance is often limited by prevailing cultural practices highlighting the need for inclusion of cultural anthropologists and sociologists or others with knowledge of local cultures in the outbreak response team.25 Ebola in Infants and Children Although children become infected with EBOV (indeed, the suspected first case of the current 2014 outbreak is believed to be a 2-year-old child in Guinea40), they typically comprise only a minority (approximately 10%) of cases during recognized human outbreaks.10,41 The highest risk of contracting the infection is among the people who take care of ill individuals, either in a healthcare setting or at home, or those who handle the remains of individuals who have died.10 Young children are largely spared of these exposures, which may, to a large extent, explain their relatively low representation among EVD victims.42 Evidence on whether children have different disease severity or prognosis, compared with adults, is limited. In a report summarizing the pediatric burden of EVD during an outbreak in the Northern Uganda, Gulu district, in 2000–2001 caused by SUDV, 20 of 218 (9%) of laboratory-confirmed cases were in children less than 18 years of age; their mean age was 8.2 years, and 35% of them were under 5 years of age. Among these children, the case fatality was 40%, whereas the overall case fatality for that outbreak was 50%. There was a slight female preponderance among infected children (M:F, 3:4).41 All Ebola-positive children had fever. Other common symptoms included vomiting (70%), diarrhea (60%) and cough (65%). Prolonged close contact with an infected relative was associated with fatality.41 Further analysis of case fatality of all laboratory-confirmed cases in children from that outbreak revealed that children 59 years of age. In the same outbreak, 7.5% of case patients were children or adolescents  <16 years of age.17 In the current 2014 EBOV outbreak, and as of mid-September 2014, children less than 15 years of age comprise approximately 14% of all reported confirmed and probable EVD cases6 ; case fatality for children <15 years of age was 73.4%, 66.1% among those 15–44 years of age and 80.4% among those older than 45 years.6 It has not been reported how many cases are in neonates or infants. The findings from the current outbreak, taken together with those of the 1995 Kikwit and 2001 Gulu outbreaks (the latter was caused by SUDV, whereas the 1995 and 2014 outbreaks were caused by EBOV), may indicate that children, adolescents and young adults have lower fatality from EVD, compared with older adults.Neonatal case fatality of EVD appears to be very high. Neonates born to mothers with EVD have not survived; in the 1976 outbreak in Zaire, which was linked to receipt of injections using contaminated needles and where a disproportionately high proportion of EBOV infected EBOV infected women were pregnant, there were 11 neonates born to mothers with EVD; all died within 19 days of life.43 The causes of these deaths are uncertain; 7 of the 11 neonates had fever.43 Subsequent outbreaks have confirmed high neonatal fatality.44 SUDV has been detected in breast milk 15 days after disease onset27; however, it is unknown whether these viruses can be transmitted from mothers to infants through that route.44 Breastfeeding infants of infected mothers may be at high risk.10 Anecdotal evidence from local practitioners suggests that Ebola survivors may not be able to maintain lactation after recovery (G. Risi, World Health Organization's Global Outbreak Alert and Response Network, personal communication, September 30, 2014); more information is needed. Pediatric, but not adult, survivors of SUDV infection had higher levels of the chemokine regulated on activation of normal T cell expressed and secreted (RANTES) and lower levels of plasminogen activator inhibitor 1, soluble intracellular adhesion molecule and soluble vascular adhesion molecule, compared with their counterparts who died, which may indicate differences in pathophysiology as well as potentially approaches to treatment for children versus adults.24Implications for Pediatric Clinical Care and Infection Control Because of the length of the incubation period, the potential exists for persons with incubating infection to travel from an outbreak-affected area to a distant location, as illustrated by the patients diagnosed with EVD in Dallas and in New York City.45 The following guidance applies to health care workers in the US or a similar setting; guidance is posted on the CDC website, which should be checked for updates.38 Evaluation of an acutely ill child, as always, should begin with a thorough medical history, including a travel history. If a child with an acute febrile illness has resided in or traveled to a country where there is active transmission of EVD in the preceding 3 weeks, EVD should be considered in the differential diagnosis. Of course, other febrile illnesses related to similar travel exposures, such as malaria and typhoid fever, should also be considered,46 as should febrile illnesses common in the US, with diagnostic testing as clinically indicated. A patient with an epidemiologic risk factor within the 21 days before symptom onset who has a febrile illness (with or without other symptoms of EVD) is considered a person under investigation.47–49 Infection control precautions should be employed in the initial medical evaluation (detailed on the CDC website),38,50 and public health authorities should be notified as soon as possible. Guidelines for the evaluation of exposure risk can be accessed on the CDC website.48 The case definitions for EVD on the CDC website47 apply to all age groups.If EVD is suspected, infection control precautions should be instituted immediately, if not already in place. Appropriate protocols for the isolation of suspected EVD cases and health care worker precautions are updated by the CDC in collaboration with state and local health care authorities. A full list of up-to-date infection control precautions33 and environmental infection control guidance37 can be accessed on the CDC website. Visitors should be limited to those essential to the patient's wellbeing, and all visitors, including parents, should be educated on hand hygiene and proper use of the necessary personal protective equipment.33 The duration of precautions should be determined on a case-by-case basis in conjunction with laboratory confirmation and local, state and federal health authorities.48,50Diagnostic testing capability for EVD has been established within selected state public health laboratories in the US, with confirmation of presumptive results being performed at CDC. If diagnostic testing for EVD is indicated, the state or local health department should be immediately notified. Staff collecting specimens should use all personal protective equipment indicated in the infection control precautions, including a full face shield.51 To test for EBOV, a minimum of 4 mL whole blood should be collected in a plastic collection tube and immediately stored or transported at 2–8°C or frozen on cold packs. Whole blood preserved with ethylenediaminetetraacetic acid is preferred, but whole blood preserved with sodium polyanethol sulfonate, citrate or with clot activator is acceptable.51 Specimens should not be submitted to the CDC in glass containers or heparinized tubes nor should samples be sent without prior consultation. If short-term specimen storage is necessary before shipment, the specimen should be frozen or stored at 4°C. Confirmation of acute infections is performed by real time RT-PCR assay in a Clinical Laboratory Improvement Amendments-certified laboratory. Detailed instructions on packaging and shipping specimens can be accessed on the CDC website51; the state and/or local health departments need to be involved when EVD diagnostic testing are considered, and CDC needs to be notified before specimens are sent.CONCLUSIONS The current outbreak of EVD in West Africa is the largest in history greater than one in duration, and more than 8 months into the outbreak numbers of new reported cases and deaths continue to rise.6 Large increases in population size, increased urbanization with human penetration into previously remote areas of forest and better connectivity of the population internally and across country borders likely contributed to this change.8 If drastic measures to curb it are not taken, the current outbreak could increase by many orders of magnitude, and EVD could even become endemic.6 The main control measures to prevent EBOV spread include isolation of cases, improved contact tracing, increased capacity for clinical care, safe funeral practices, greater community engagement and trust, support from international partners and the availability of an efficacious vaccine.6 Currently, a major international effort is being undertaken in aiding the local response, educating healthcare personnel and the public on infection control practices and establishing treatment facilities in the hopes of increasing survival rates and slowing disease transmission. Evidence-based responses that are adapted to the affected communities52 are necessary to combat this epidemic, as are efforts to support the affected countries’ healthcare systems so that they can respond both to the EVD epidemic and to the many other pressing health needs of the local populations. The current outbreak can provide the opportunity to improve our understanding of EVD in children by systematically collecting information on disease course and predictors of survival in children of different ages. This could be accomplished through the development and implementation of uniform data collection forms on patient and disease characteristics for those treated at Ebola treatment centers, through the collaboration of local ministries of health and international relief organizations. Information on length of viral shedding in different secretions (including saliva, breast milk and genital secretions) and their potential to transmit disease is also needed to help inform guidance on preventing secondary transmission of EVD.REFERENCES 1. Curtis, N. Viral hemorrhagic fevers caused by Lassa, Ebola and Marburg viruses.. In: Pollard, AJ.; Finn, A., editors. Hot Topics in Infection and Immunity in Children. Springer; New York: 2006. p. 35-44. 2. Centers for Disease Control and Prevention (CDC). [November 30, 2014] Outbreaks chronology: Ebola virus disease. 2014. Available at: http://www.cdc.gov/vhf/ebola/outbreaks/history/ chronology.html. 3. Bray M. Epidemiology, pathogenesis, and clinical manifestations of Ebola and Marburg virus diseases. Sep.2014 18:2014. 4. Frieden TR, Damon I, Bell BP, et al. Ebola 2014—new challenges, new global response and responsibility. N Engl J Med. 2014; 371:1177–1180. [PubMed: 25140858] 5. Centers for Disease Control and Prevention (CDC). [November 30, 2014] 2014 Ebola outbreak in West Africa—case counts. 2014. Available at: http://www.cdc.gov/vhf/ebola/outbreaks/2014-westafrica/case-counts.html. 6. Team WHOER. Ebola virus disease in West Africa—the first 9 months of the epidemic and forward projections. N Engl J Med. 2014; 371:1485–1491. 7. World Health Organization (WHO). [November 30, 2014] WHO: Ebola response roadmap situation report. 2014. Available at: http://apps.who.int/iris/bitstream/10665/133833/1/ roadmapsitrep4_eng.pdf?ua=1. 8. Pigott DM, Golding N, Mylne A, et al. Mapping the zoonotic niche of Ebola virus disease in Africa. Elife. 2014; 3:e04395. [PubMed: 25201877] 9. Peters, CJ. Marburg and Ebola virus hemorrhagic fever.. In: Mandell, GL.; Bennett, JE.; Dolin, R., editors. Principles and Practice of Infectious Diseases. 7th ed.. Churchill Livingstone/Elsevier; Philadelphia: 2010. p. 2259-2263. 10. Bell, M. Ebola and Marburg hemorrhagic fever viruses.. In: Long, SS.; Pickering, LK.; Prober, CG., editors. Principles and Practice of Pediatric Infectious Disease. 3rd ed.. Churchill Livingstone/Elsevier; Philadelphia: 2008. p. 1138-1139. 11. Dowell SF, Mukunu R, Ksiazek TG, Khan AS, Rollin PE, Peters CJ. Transmission of Ebola hemorrhagic fever: a study of risk factors in family members, Kikwit, Democratic Republic of the Congo, 1995. Commission de Lutte contre les Epidemies a Kikwit. J Infect Dis. 1999; 179(Suppl 1):S87–S91. [PubMed: 9988169] 12. Ksiazek TG, Rollin PE, Williams AJ, et al. Clinical virology of Ebola hemorrhagic fever (EHF): virus, virus antigen, and IgG and IgM antibody findings among EHF patients in Kikwit, Democratic Republic of the Congo, 1995. J Infect Dis. 1999; 179(Suppl 1):S177–S187. [PubMed: 9988182] 13. Tomori O, Fabiyi A, Sorungbe A, et al. Viral hemorrhagic fever antibodies in Nigerian populations. Am J Trop Med Hyg. 1988; 38:407–410. [PubMed: 3128130] 14. Centers for Disease Control and Prevention (CDC). Estimating the future number of cases in the ebola epidemic—Liberia and Sierra Leone, 2014–2015. MMWR Surveill Summ. 2014; 63:1–14. 15. Pourrut X, Délicat A, Rollin PE, et al. Spatial and temporal patterns of Zaire ebolavirus antibody prevalence in the possible reservoir bat species. J Infect Dis. 2007; 196(Suppl 2):S176–S183. [PubMed: 17940947] Kourtis et al. Page 9 Pediatr Infect Dis J. Author manuscript; available in PMC 2016 August 01. Author Manuscript Author Manuscript Author Manuscript Author Manuscript 16. Leroy EM, Kumulungui B, Pourrut X, et al. Fruit bats as reservoirs of Ebola virus. Nature. 2005; 438:575–576. [PubMed: 16319873] 17. Khan AS, Tshioko FK, Heymann DL, et al. The reemergence of Ebola hemorrhagic fever, Democratic Republic of the Congo, 1995. Commission de Lutte contre les Epidemies a Kikwit. J Infect Dis. 1999; 179(Suppl 1):S76–S86. [PubMed: 9988168] 18. World Health Organization (WHO). [October 16, 2014] WHO: Ebola response roadmap situation report—15 October. 2014. Available at: http://apps.who.int/iris/bit-stream/10665/136508/1/ roadmapsitrep15Oct2014.pdf?ua=1. 19. Breman JG, Johnson KM. Ebola then and now. N Engl J Med. 2014; 371:163–166. 20. Wamala JF, Lukwago L, Malimbo M, et al. Ebola hemorrhagic fever associated with novel virus strain, Uganda, 2007–2008. Emerg Infect Dis. 2010; 16:1087–1092. [PubMed: 20587179] 21. Centers for Disease Control and Prevention (CDC). Ebola viral disease outbreak—West Africa, 2014. MMWR Morb Mortal Wkly Rep. 2014; 63:548–551. [PubMed: 24964881] 22. Mupapa K, Mukundu W, Bwaka MA, et al. Ebola hemorrhagic fever and pregnancy. J Infect Dis. 1999; 179(Suppl 1):S11–S12. [PubMed: 9988157] 23. McElroy AK, Erickson BR, Flietstra TD, et al. Ebola hemorrhagic fever: novel biomarker correlates of clinical outcome. J Infect Dis. 2014; 210:558–566. [PubMed: 24526742] 24. McElroy AK, Erickson BR, Flietstra TD, et al. Biomarker correlates of survival in pediatric patients with Ebola virus disease. Emerg Infect Dis. 2014; 20:1683–1690. [PubMed: 25279581] 25. Bray M. Diagnosis and treatment of Ebola and Marburg virus disease. 2014 26. Rowe AK, Bertolli J, Khan AS, et al. Clinical, virologic, and immunologic follow-up of convalescent Ebola hemorrhagic fever patients and their household contacts, Kikwit, Democratic Republic of the Congo. Commission de Lutte contre les Epidémies à Kikwit. J Infect Dis. 1999; 179(Suppl 1):S28–S35. [PubMed: 9988162] 27. Bausch DG, Towner JS, Dowell SF, et al. Assessment of the risk of Ebola virus transmission from bodily fluids and fomites. J Infect Dis. 2007; 196:S142–147. [PubMed: 17940942] 28. Rodriguez LL, De Roo A, Guimard Y, et al. Persistence and genetic stability of Ebola virus during the outbreak in Kikwit, Democratic Republic of the Congo, 1995. J Infect Dis. 1999; 179(Suppl 1):S170–176. [PubMed: 9988181] 29. Qiu X, Wong G, Audet J, et al. Reversion of advanced Ebola virus disease in nonhuman primates with ZMapp. Nature. 2014; 514:47–53. [PubMed: 25171469] 30. Fauci AS. Ebola—underscoring the global disparities in health care resources. N Engl J Med. 2014; 371:1084–1086. [PubMed: 25119491] 31. Geisbert TW. Medical research: Ebola therapy protects severely ill monkeys. Nature. 2014; 514:41–43. [PubMed: 25171470] 32. WHO.. [October 15, 2014] Consultation on potential Ebola therapies and vaccines—background document for participants. 2014. Available at: http://www.who.int/csr/disease/ebola/ebola-newinterventions-02-sep-2014.pdf?ua=1. 33. Centers for Disease Control and Prevention (CDC). [September 19, 2014] Infection prevention and control recommendations for hospitalized patients with known or suspected Ebola hemorrhagic fever in US hospitals. 2014. Available at: http://www.cdc.gov/vhf/ebola/hcp/infection-preventionand-control-recommendations.html. 34. Mupapa K, Massamba M, Kibadi K, et al. Treatment of Ebola hemorrhagic fever with blood transfusions from convalescent patients. International Scientific and Technical Committee. J Infect Dis. 1999; 179(Suppl 1):S18–S23. [PubMed: 9988160] 35. Sadek RF, Khan AS, Stevens G, Peters CJ, Ksiazek TG. Ebola hemorrhagic fever, Democratic Republic of the Congo, 1995: determinants of survival. J Infect Dis. 1999; 179(Suppl 1):S24–27. [PubMed: 9988161] 36. World Health Organization (WHO). [September 22, 2014] Statement on the WHO consultation on potential Ebola therapies and vaccines. 2014. Available at: http://www.who.int/mediacentre/news/ statements/2014/ebola-therapies-consultation/en/. 37. Centers for Disease Control and Prevention (CDC). [September 28, 2014] Interim guidance for environmental infection control in hospitals for Ebola virus. 2014. Available at: http:// www.cdc.gov/vhf/ebola/hcp/environmental-infection-control-inhospitals.html. 38. Centers for Disease Control and Prevention (CDC). [November 10, 2014] Interim guidance for the U.S. residence decontamination for Ebola virus disease (Ebola) and removal of contaminated waste. 2014. Available at: http://www.cdc.gov/vhf/ebola/hcp/residental-decontamination.html. 39. Borchert M, Mutyaba I, Van Kerkhove MD, et al. Ebola haemorrhagic fever outbreak in Masindi District, Uganda: outbreak description and lessons learned. BMC Infect Dis. 2011; 11:357. [PubMed: 22204600] 40. Baize S, Pannetier D, Oestereich L, et al. Emergence of Zaire Ebola virus disease in Guinea. N Engl J Med. 2014; 371:1418–1425. [PubMed: 24738640] 41. Mupere E, Kaducu OF, Yoti Z. Ebola haemorrhagic fever among hospitalised children and adolescents in northern Uganda: epidemiologic and clinical observations. Afr Health Sci. 2001; 1:60–65. [PubMed: 12789118] 42. Dowell SF. Ebola hemorrhagic fever: why were children spared? Pediatr Infect Dis J. 1996; 15:189–191. [PubMed: 8852904] 43. World Health Organization (WHO). Ebola haemorrhagic fever in Zaire, 1976. Bull World Health Organ. 1978; 56:271–293. [PubMed: 307456] 44. Jamieson DJ, Uyeki TM, Callahan WM, et al. What obstetricians–gynecologists should know about Ebola; a perspective from the Centers for Disease Control and Prevention. Obst Gynecol. 2014; 124:1005–1010. [PubMed: 25203368] 45. Chevalier MS, Chung W, Smith J, et al. Centers for Disease Control and Prevention (CDC). Ebola virus disease cluster in the United States—Dallas County, Texas, 2014. MMWR Morb Mortal Wkly Rep. 2014; 63:1087–1088. [PubMed: 25412069] 46. Wilson, ME. Fever in returned travelers.. In: Brunette, GW.; Kozarsky, PE., editors. CDC Health Information for International Travel 2014. Oxford University Press; New York, NY: 2014. 47. Centers for Disease Control and Prevention (CDC). [November19, 2014] Case definition for Ebola virus disease. 2014. Available at: http://www.cdc.gov/vhf/ebola/hcp/case-definition.html. 48. Centers for Disease Control and Prevention (CDC). [November 30, 2014] Interim guidance for monitoring and movement of persons with Ebola virus disease exposure. 2014. Available at: http:// www.cdc.gov/vhf/ebola/hcp/monitoring-and-movement-of-persons-with-exposure.html. 49. Centers for Disease Control and Prevention (CDC). [November 10, 2014] Epidemiologic risk factors to consider when evaluating a person for exposure to Ebola virus. 2014. Available at: http://www.cdc.gov/vhf/ebola/exposure/risk-factors-when-evaluating-person-for-exposure.html. 50. Centers for Disease Control and Prevention (CDC). [November 10, 2014] When caring for suspect or confirmed patients with Ebola. Available at: http://www.cdc.gov/vhf/ebola/hcp/caring-forebola-suspects.html. 51. Centers for Disease Control and Prevention (CDC). [November 15, 2014] Interim guidance for specimen collection, transport, testing, and submission for persons under investigation for ebola virus disease in the United States. 2014. Available at: http://www.cdc.gov/vhf/ebola/hcp/interimguidance-specimen-collection-submission-patients-suspected-infection-ebola.html. 52. Eba PM. Ebola and human rights in West Africa. Lancet. 2014; 384:2091–2093. [PubMed: 25245179]

AbstractDengue viruses (DENVs) cause the most common arthropod-borne viral disease in man with 50–100 million infections per year. Because of the lack of a vaccine and antiviral drugs, the sole measure of control is limiting the Aedes mosquito vectors. DENV infection can be asymptomatic or a self-limited, acute febrile disease ranging in severity. The classical form of dengue fever (DF) is characterized by high fever, headache, stomach ache, rash, myalgia, and arthralgia. Severe dengue, dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS) are accompanied by thrombocytopenia, vascular leakage, and hypotension. DSS, which can be fatal, is characterized by systemic shock. Despite intensive research, the underlying mechanisms causing severe dengue is still not well understood partly due to the lack of appropriate animal models of infection and disease. However, even though it is clear that both viral and host factors play important roles in the course of infection, a fundamental knowledge gap still remains to be filled regarding host cell tropism, crucial host immune response mechanisms, and viral markers for virulence.Keywords: dengue virus, dengue fever, dengue hemorrhagic fever, dengue shock syndrome, flavivirus, vector-borne virus, arbovirus

Considering the importance of dissolved organic carbon (DOC) flows for the carbon biogeochemical cycle, and a set of organic matter (OM) ecosystem services, our work aimed to analyze and discuss water DOC concentrations from different forest compartments: bulk precipitation, throughfall, soil solution, and stream water, in a mountainous rainforest in southeastern Brazil (Atlantic Forest). A hillslope-scale spatial design aimed to add to the discussion an analysis linked to the litter decomposition heterogeneity observed between different hillslope positions for DOC leaching. A temporal analysis was carried out by comparing rainfall events, which are different about their rainfall characteristics and antecedent humidity context. A dilution effect associated with rainfall intensity was observed in wet and dry depositions, being more pronounced on the dry deposition, which also showed a pre-wash effect linked to the previous rainfall-volume, with the time range of 15-days of previous rainfall as more relevant. Under-litter DOC concentrations showed no dilution or pre-wash effects. While in the throughfall there was no spatial difference in a hillslope-scale, the litter leaching showed great spatial variation, so that the intermediate stocks (and decomposition rates) of the mid-hillslope areas presented higher concentrations, which it is due to a balance between accumulation of material on the soil (little loss by microbiota respiration) and chemical rework on the material (new solubles) that favors the DOC leaching. In the soil solution, there is a tendency to decrease concentrations in depth. However, in events with greater rainfall intensity, soil packages with a higher OM incorporated can change from an adsorption environment to a desorption environment. The stream water showed, under baseflow condition, lower concentrations of DOC than observed in the bulk precipitation, highlighting the soil role for the organic carbon retention, where a high water infiltration capacity and OM decomposition efficiency may have key-role.

By increasing load demands and extending power networks to response customers need the complexity and integration of power systems have been boosted which increases the short circuit current level of the system that may be a threaten for network’s reliability. Over these years, some approaches have been proposed to deal with this issue, reconfiguration of networks, increasing circuit breakers (CBs) capacity, and implementation of fault current limiter (FCL) is as proper examples. Reconfiguration and increasing CBs rating have applied exorbitant costs to the system and in some cases, it may be infeasible. Hence, FCLs can play a pivotal role in the mitigation of fault current level, but the effectiveness of FCLs is depended to the numbers and impedance of FCLs. In this paper, a novel and multi-objective approach are presented to optimize three objective functions including decreasing short circuit level, increasing the systems reliability level, and minimizing costs of FCL installations. Adaptive penalty factor and Pareto based Multi objective Evolutionary Algorithm Based on Decomposition (MOEA/D) is used to optimize the aforementioned objectives. Numerical and graphical results of optimization studies in MATLAB software on IEEE RTS 24-Bus system are confirmed the proposed approach efficiency.

Dibutyl phthalate (DBP) is an environmental pollutant that can threaten human health. The strain Arthrobacter sp. ZJUTW, isolated from the sludge of river of Hangzhou city, can efficiently degrade DBP. Its genomic and transcriptomic differences when cultivated with DBP and with glucose revealed specific DBP metabolic pathways in the ZJUTW strain. The degrading gene clusters distribute separately on a circular chromosome and a plasmid pQL1. Genes related to the initial steps of DBP degradation from DBP to phthalic acid (PA), the pehA gene and pht gene cluster, are located on the plasmid pQL1. While pca gene cluster related to the transforming of protocatechuic acid (PCA) to acetyl-CoA, is located on the chromosome. After homologous alignment analysis with the reported gene clusters, we found that there were a series of double copies of homologous genes in pht and pca gene clusters that contribute to the efficient degradation of DBP by ZJUTW. In addition, transcriptomic analysis showed a synergistic effect between pht and pca clusters, which also favor ZJUTW allowing it to efficiently degrade DBP. Combined genomic and transcriptomic analyses affords the complete DBP metabolic pathway in Arthrobacter sp. ZJUTW that is different from that of reported other Arthrobacter strains. After necessary modification based on its metabolic characteristics, Arthrobacter sp. ZJUTW or its mutants might represent promising candidates for use in the bioremediation of DBP pollution.

Secondary contact between closely related species can lead to the formation of hybrid zones, allowing for interspecific gene flow among taxa. Species replacement can take place if one of the species possesses a competitive advantage over the other, resulting in hybrid zone movement. This displacement may leave a genomic footprint across the landscape in the form of asymmetric introgression of selectively neutral alleles from the displaced to the advancing species. Hybrid zone movement has been suggested for marbled newts in the Iberian Peninsula, supported by the presence of a Triturus marmoratus stronghold surrounded by populations of the supposedly advancing T. pygmaeus in the northwest of the Lisbon Peninsula, i.e., an enclave. Moreover, a newly constructed two-species distribution model suggests that climate conditions following the Last Glacial Maximum may have favoured T. pygmaeus over T. marmoratus along the Atlantic coast. To test for the presence of a T. marmoratus genomic footprint in the area that may have witnessed species displacement, we developed and employed 54 nuclear SNPs and one mitochondrial DNA marker. We found no additional enclaves nor genetic traces of T. marmoratus in T. pygmaeus populations. Therefore, two main hypothesis arise in the absence of a genomic footprint: i) species replacement without hybridisation, either in allopatry or in sympatry under strong reproductive isolation; or ii) displacement with hybridisation where the footprint was eroded due to strong purifying selection. We predict testing for a genomic footprint north of the reported enclave could confirm that species replacement in the marbled newts occurred with hybridisation.

PtrWRKY75, PtrPAL1, poplar, drought tolerance, reactive oxygen species, salicylic acid, stomatal closure

An Adaptive Unscented Kalman Filter (AUKF) method combining sensor fusion algorithm with Artificial Neural Network (ANN) is designed for high precision attitude tracking of low cost, small size Micro-Electro-Mechanical System (MEMS) Inertial Measurement Unit (IMU) in high dynamic environment. The different control strategies fusing multi MEMS inertial sensors are adopted under various dynamic situations. The AUKF attitude estimation approach utilizing the MEMS sensor and Global Positioning System (GPS) could provide reliable estimation in high dynamic environmental variations. The adaptive scale factor is used to adaptively weaken or enhance the effects on new measurement data through the adjustment of the estimation according to the predicted residual vector. To solve the problem that new measurement data could not be updated in case of GPS failure situation, an attitude algorithm based on RBF-ANN feedback correction is proposed to apply in AUKF. The estimated deviation of predicted non-augmented system state would be provided based on Radial Basis Function (RBF)-ANN. The corrected the predicted non-augmented system state would be used for estimation process in AUKF. The experiment platform simulating the rotation of spinning projectile the was setup. The comparative experimental results show better control performance of the proposed method under various dynamic conditions.

The fifth order short pulse equation models the nonlinear propagation of optical pulses of a few oscillations duration in dielectric media. In particular, it models the propagation of circularly and elliptically polarized few-cycle solitons in a Kerr medium. In this paper, we prove the well-posedness of the classical solutions for the Cauchy problem associated with this equation.

In this paper, we have considered two hybrid systems of FDEs for the existence results and stability criteria. The problems are more general than considered in the literature and to the best of our study in the field, no one considered singular hybrid-FDE with p-Laplacian operator for the existence and stability results. We utilize the well known Guo-Krasnoselskii's fixed point theorem.

In this paper, we investigate the properties of involutes of singular spherical curves. In general, the involute of a regular spherical curve has singularities, hence we consider Legendre curves in the unit spherical bundle. By using the moving frame and the curvature of fronts, we define involutes of fronts in the Euclidean 2-sphere. We give some properties of involutes at singular points. Moreover, we consider the relationships between evolutes and involutes of fronts without inflection points and give a kind of four vertices theorem. Furthermore, by the definition of pedal curves, we define contrapedal curves of fronts in the Euclidean 2-sphere and give some relationships between them.

In this study, we construct ruled surfaces whose Disteli-axis is constant in dual 3-space D^3_1 . Then we attain a general system characterizing these surfaces, and also give characterizations for a ruled surface to get a constant Disteli-axis. As a result, the ruled surface formed by a line undergoing a screw motion is investigated.

Temporal partitioning is an important mechanism for carnivore mammals that live in sympatry in current forest remnants. We evaluated whether temporal partitioning would facilitate coexistence among carnivores in a tropical forest and its adjacent human-related area, as well as if there is a possible correlation between the activity patterns of these carnivores and their potential prey. We used camera traps and circular statistics to explore the degree of temporal overlap between dominant and subordinate predators, as well as between predators and their potential preys. Pumas (Puma concolor) were less active when jaguars (Panthera onca) were more active. Overall, ocelots (Leopardus pardalis) and crab-eating foxes (Cerdocyon thous) presented either a strong or a weak temporal partitioning with jaguars and pumas, respectively, but apparently spatial or dietary segregation might facilitate more their coexistence with these large predators. Tayras (Eira barbara) and coatis (Nasua nasua) were diurnal and, therefore, did not overlap temporally with nocturnal carnivores, except pumas. In the human-related area, ocelots were mostly nocturnal and pumas diurnal, probably due to the temporal activity of their related preys. Our findings suggest that temporal partitioning may allow coexistence between our studied predators in one of the largest Atlantic Forest remnant in Brazil, but preys have an important role, shifting the activity pattern of their predators according to the studied area.

Mine reclamation in the Athabasca oil sands region Canada, is required by law where companies must reconstruct disturbed landscapes into functioning ecosystems such as forests, wetlands and lakes that existed in the Boreal landscape prior to mining. Winter is a major hydrological factor in this region as snow covers the landscape for 5 to 6 months and is ~25% of the annual precipitation, yet few studies have explored the influence of winter processes on the hydrology of constructed watersheds. One year (2017-2018) of intensive snow hydrology measurements are supplemented with six years (2013-2018) of meteorological measurements from the constructed Sandhill Fen Watershed to: 1) understand snow accumulation and redistribution, snowmelt timing, rate and partitioning, 2) apply a physically-based model for simulating winter processes on hillslopes and 3) evaluate the impact of soil prescriptions and climate change projections on winter processes in reclaimed systems. The 2017-2018 snow season was between November and April and SWE ranged between 40-140 mm. Snow distribution was primarily influenced by topography with little influence of snow trapping from developing vegetation. Snow accumulation was most variable on hillslopes and redistribution was driven by slope position, with SWE greatest at the base of slopes and decreased towards crests. Snowmelt on hillslopes was controlled by slope aspect, as snow declined rapidly on west and south-facing slopes, compared to east and north-facing slopes. Unlike results previously reported on constructed uplands, snowmelt runoff from uplands was much less (~30%), highlighting the influence of different construction materials. Model simulations indicate that antecedent soil moisture and soil temperature have a large influence on partitioning snowmelt over a range of observed conditions. Under a warmer and wetter climate, average annual peak SWE and snow season duration could decline up to 52 % and up to 61 days, respectively while snowmelt runoff ceases completely under the warmest scenarios. Results suggest considerable future variability in snowmelt runoff from hillslopes, yet soil properties can be used to enhance vertical or lateral flows.

Small mammal abundances are frequently limited by resource availability but predators can exert strong lethal (direct mortality) and non-lethal limitations (e.g. depressed site-level activity). Artificially increasing resource availability for small mammals provides a unique opportunity to examine predator-prey interactions. We monitored the 3-year response of arboreal rodents and their predators at nest platforms (n = 598; 23 young forest sites), using annual inspections and remote cameras (n = 168). One year after adding nest platforms we found a 2.9 to 9.2-fold increase in red tree vole (Arborimus longicaudus) use at the site-level, but little use by potential predators. Predator use of nest platforms began in year two and increased in year three of the study. Most potential nest predators were positively correlated with tree vole presence at nest platforms but effect size and direction varied with temporal grain considered (e.g. hour vs day time-bin widths). Flying squirrels (Glaucomys humboldtensis) were positively correlated with disturbances caused by digging birds. Using a Cormack-Jolly-Seber model and encounter histories produced from visual re-captures of marked tree voles, we estimated apparent annual survival to be 0.099 ± 0.057 (x̄ ± 1 SE) for females and 0.005 ± 0.014 for males. Weasels (Mustela spp.), an active seeking predator, preyed upon tree voles most frequently with 10% of weasel detections resulting in mortality of a tree vole (n = 8) whereas owls, an ambush predator, did not prey upon tree voles at nest platforms even though they were detected at similar frequencies as weasels. Weasels also exerted potential non-lethal effects and we observed a >10-fold reduction in the number of tree vole detections per week after weasel detection. Our evidence indicates that predators exert direct and indirect effects on tree vole populations with active seeking predators being the most important predators at nest sites.

We seek to explain why the hydrogen bond possesses unusual strength in small water clusters that account for many of the complex behaviors of water. We have investigated and visualized the donation of covalent character from covalent (sigma) to hydrogen-bonds, by calculating the eigenvector coupling properties of QTAIM, stress tensor σ(r) and Ehrenfest Force F(r) on the F(r) molecular graph. The next generation 3-D bond-path framework sets are presented and only the F(r) bond-path framework sets reproduce the earlier finding on the coupling between covalent (sigma) and hydrogen-bonds that possess a degree of covalent character. The directional character of the covalent (sigma) and hydrogen-bonds 3-D bond-path framework sets for the F(r) explains differences found in the earlier results from QTAIM and the stress tensor σ(r).

Pipeline transmission is one of the most important ways of oil and gas transportation, and its safety is majorly threatened by fatigue fracture that generally occurs in heat-affected zone (HAZ) adjacent to the welded joint of the pipeline. Therefore, studying the fatigue properties of HAZ is important. In this work, the microstructure and mechanical properties in the HAZ of a X80 pipe were accurately simulated by thermal simulation. The fatigue life and crack growth rate of typical sub-HAZ were tested. Results showed that the fine grain HAZ had the lowest strength and fatigue life. By contrast, the coarse grain HAZ had the highest strength, but its fatigue life was lower than that of the intercritical HAZ. Furthermore, the microstructure of each sub-HAZ and its effect on fatigue properties were discussed in detail. The results will reveal the effects of microstructure and mechanical properties on the service safety of pipeline transportation.

Biodiversity is under threat worldwide. Over the past decade, the field of population genomics has developed across non-model organisms, and the results of this research have begun to be applied in conservation and management of wildlife species. Genomics tools can provide precise estimates of basic features of wildlife populations, such as effective population size, inbreeding, demographic history, and population structure, that are critical for conservation efforts. Moreover, population genomics studies can identify particular genetic loci and variants responsible for inbreeding depression or adaptation to changing environments, allowing for conservation efforts to estimate the capacity of populations to evolve and adapt in response to environmental change and to manage for adaptive variation. While connections from basic research to applied wildlife conservation have been slow to develop, these connections are increasingly strengthening. Here we review the primary areas in which population genomics approaches can be applied to wildlife conservation and management, highlight examples of how they have been used, and provide recommendations for building on the progress that has been made in this field.

1. Understanding how invasive species respond to novel environments is limited by a lack of sensitivity and throughput in conventional biomonitoring methods. Arthropods in particular are often difficult to monitor due to small size, rapid lifecycles, and/or visual similarities with co-occurring species. This is true for the agromyzid leafminer, Liriomyza sativae, a global pest of vegetable and nursery industries that has recently established in Australia. 2. A highly robust method based on environmental DNA (eDNA) was developed exploiting traces of DNA left inside ‘empty’ leaf mines, which are easier to collect and persist longer in the environment than the insect. This extended the window of possible diagnosis to at least 28 days since a leaf mine became empty. The test allowed for visually indistinguishable leafmining damage caused by L. sativae to be genetically differentiated from that of other flies. 3. Field application resulted in the identification of new local plant hosts for L. sativae, including widely distributed weeds and common garden crops, with important implications for the pest’s ability to spread. Moreover, the test allowed for the confirmation of L. sativae on an island with a previously unconfirmed population. 4. The developed eDNA method is likely to become an important tool for L. sativae and other leafmining species of biosecurity significance, which, historically, have been difficult to detect, diagnose and monitor. More generally, eDNA is emerging as a highly sensitive and labour-efficient surveillance tool for difficult to survey species to improve outcomes for agricultural industries, global health, and the environment.