text:
The Ministry of Trade, Industry and Energy and the Korea Association of Machinery Industry announced on Aug. 21 that South Korea's material and component exports totaled US$114,528 million, with a year-on-year decline of 10.3 percent, for the first five months of this year.
Specifically, electronic component exports dropped 22.1 percent and metal processing product exports, chemical substance and product exports, and textile product exports fell 17.5 percent, 9.7 percent, and 2.1 percent, respectively. On the other hand, general machine component exports, rubber and plastic product exports, precision equipment component exports, and transport machinery component exports rose 6.8 percent, 4.7 percent, 3.7 percent, and 2.2 percent, respectively.
South Korea's material and component exports to China added up to US$33,172 million and those to the United States totaled US$12,881 million. The exports to the two countries accounted for approximately 30 percent of the total. Those to China, the largest trade partner, decreased no less than 18.8 percent with China's demands falling due to its trade war with the United States. South Korea's total material and component exports fell more than 10 percent as a result.
Those to the United States rose 2.8 percent and those to Vietnam jumped 9.1 percent to US$11,315 million. Vietnam has become the third-largest export destination for South Korean material and component suppliers. Their exports to Japan fell 6.3 percent on year to US$5,499 million.
During the same period, South Korea's material and component imports reached US$72,376 million, down 1.4 percent from a year ago. Metal processing product imports, precision equipment component imports, textile product imports, chemical substance and product imports, and general machine component imports decreased 16.4 percent, 8 percent, 7.1 percent, 5.6 percent, and 5.2 percent, respectively. Electronic component imports, rubber and plastic product imports, and nonmetallic mineral product imports increased 3.4 percent, 2.7 percent, and 2.3 percent, respectively. Imports from China added up to US$23,104 million, followed by those from Japan (US$11,140 million).
From January to May this year, South Korea's material and component imports from Japan went down 8.4 percent while its total material and component imports edged down 1.4 percent. As a result, the ratio of the imports from Japan to the total imports decreased from 16.6 percent to 15.4 percent.
During the period, South Korea posted a trade surplus of US$42,152 million in the materials and components industry, led by its US$4,668 million surplus with the United States and US$10,068 million surplus with China. At the same time, its trade deficit with Japan in the industry amounted to US$5,641 million, bigger than any of the other deficits. For reference, South Korea's second-largest trade deficit in the industry, US$1,806 million, was with Taiwan.


text:
The English Civil War Begins
In 1642, six months before Edgehill, the first battle of the English Civil War, Charles I made two attempts to enter the city of Hull to seize control of its armoury but was refused entry on both occasions by its governor Sir John Hotham. The king's army was forced to retreat, probably making their way to Hessle, a royalist stronghold, while the disgruntled king declared Hotham a traitor.
By the 22nd of August, King Charles moved on to the City of Nottingham. Here he raised his royal standard thus marking the beginning of the English Civil War.
Execution of Charles I
The weather in January of 1649 was bitterly cold, it was not a good day for an execution, especially when the man standing on the scaffold was the king of England.
On the 30th King Charles waited inside the Banqueting House in Whitehall for the doors to be opened so that he might make his way to the scaffold that had been erected outside. Maybe there was ice on the windows, as history tells us Charles asked to wear two heavy shirts so that he might not shiver in the cold. Charles did not wish that his people think that he was afraid.
Charles I was beheaded that day - he said:
"... truly I desire their liberty and freedom as much as anybody whomsoever; but I must tell you that their liberty and freedom consist in having of government, those laws by which their life and their goods may be most their own. It is not for having share in government, sirs; that is nothing pertaining to them; a subject and a sovereign are clear different things. And therefore until they do that, I mean that you do put the people in that liberty, as I say, certainly they will never enjoy themselves. Sirs, it was for this that now I am come here. If I would have given way to an arbitrary way, for to have all laws changed according to the power of the sword, I needed not to have come here; and therefore I tell you (and I pray God it be not laid to your charge) that I am the martyr of the people..."
An observer in the crowd said of the execution:
'There was such a groan by the thousands then present as I never heard before and desire I may never hear again'.
Poor Charles, yes he was his own worst enemy, but did he deserve a death such as this?
Battle of Rowton Moor
On the 24th September in 1645 The Battle of Rowton Moor - a Parliamentarian victory.
King Charles viewed the battlefield from the Phoenix Tower (it's often now referred to as the King Charles' Tower) on the north/east corner of Chester City walls. From this vantage point, the king witnessed the defeat of the last of his cavalry.
By the middle of the seventeenth, the tower had fallen into a dilapidated state. Largely due to the battering it had received during the Civil War siege, the upper parts of the tower had to be rebuilt.
Meditations Amonget the Tombs
While researching the reign of Charles I, I discovered that in 1813 Sir Henry Halford, King George IV's physician was asked to examine the body of Charles I. He found the skin was discoloured, the nose was missing, and only a single eye and ear apparently remained. What a gruesome pass time!
Charles was laid to rest in a vault at St Georges Chapel at Windsor, (because permission was refused for his burial at Westminster Abbey) where the coffin of Henry VIII was interred. On entering the vault it was noted that Henry VIII's coffin had been damaged, he supposed that this may have been a result of a hasty burial, speculating that the lowering of his coffin caused it to crash into that of the Tudor king.
The 1813 sketch seen here is titled Meditations Amonget the Tombs by the brilliant satirical illustrator George Cruikshank pokes fun at the whole thing.
Battle of Naseby
The Battle of Naseby was fought this day in 1645.
It was the key battle of the first English Civil War and a decisive defeat for the Royalist forces.
"After Hastings and the Battle of Britain, which respectively began and ended the last millennium, Naseby was arguably the most important and decisive battle ever fought in England. Where those other battles were the result of challenges to the very basis of the kingdom by foreign foes, Naseby was the culmination of a bloody Civil War and the stepping stone for a political revolution."
Execution of Thomas Wentworth
Many issues dominated parliament during the reign of Charles I but it would be religion that would prove to be the most divisive issue that both Charles and Parliament would have to deal with.
At the end of 1640, Charles had recalled the Long Parliament whose members had used this opportunity to attack men they considered enemies of the Crown, namely Thomas Wentworth and Archbishop William Laud.
Wentworth and Laud were seen as the embodiment of all that was wrong with England at this time. It was on this day in 1641 that Wentworth was executed, Laud would follow him to the scaffold four years later.
You can read a little bit more on England at this time on my website at
Death of William Laud
"Give great praise to the Lord and little Laud to the Devil" was a popular saying in the time of King Charles I, it was in reference to William Laud, Archbishop of Canterbury, who was beheaded on Tower Hill in London on this day in 1645.
William Laud was a supporter of Charles I, he believed that Charles had the God-given right to rule by divine right - a view strongly held by Charles himself. Laud was against Puritan reform of the church.
The charges brought against Laud was that he undermined the laws of England and therefore endangered the Protestant faith, however, these charges were never actually proved. Nevertheless, William Laud was convicted by a bill of attainder by Parliament instead of a jury and his execution planned for the 9th January.
Laud requested that he died by being beheaded rather than by hanging, he was buried in the chapel of St John's College, Oxford.
An etching of Laud's trial was produced at the time that quotes from Proverbs "The righteous are delivered from trouble and the wicked get into it instead" However Laud's was being praised right up to the mid 19th century, William Gladstone, who wrote a number of sermons that he would read to his servants on a Sunday said of Laud -
"Laud as a Churchman has lasted. He lives today. His opponents have mostly disappeared from off the earth. They have left consequences, but no representatives. Laud has both."
Pontefract Castle
King Charles I, who was executed this day in 1649 was not the only casualty of the Civil War, Pontefract Castle was another.
As a result of these wars this Yorkshire castle held out against three sieges. In the end though, this once mighty medieval building was, in the words of Marie Lloyd, one of the
"of the ruins that Cromwell knocked about a bit"
The Trial of Charles I Begins
On the 25th of March 1625 at Westminster Abbey Charles I was crowned King of England, he spent most of this time in a power struggle for with Parliament. By 1629 Charles had had numerous arguments with his ministers which lead him to abolish Parliament.
Charles as king, could do this under what was known as Royal Prerogative, the divine right to rule, but by the middle of the century he was wading into trouble, many people regarding him as insensitive.
The West Country, the home of my maternal ancestors, were notable Royalist, suffered at this time, the town of Barnstaple for instance, changed from Royalist to Parliamentarians and back again no fewer that four times.
The year 1649 saw a great change in the governance of England, in the January of that year the trial of Charles I had begun. The country had seen the estimated deaths from the civil wars as 84,830 killed with another 100,000 dying from war related diseases, and therefore the king was held
"guilty of all the treasons, murders, rapes, burnings, spoils, desolations, damages and mischiefs to this nation"
Charles was declared guilty on Saturday 27 January 1649 and sentenced to death and was executed by beheading on the 30th January 1649.
The English Civil War Begins.
It was on this day in 1642, that King Charles I, accompanied by a number of soldiers, arrived at Westminster with the intent to arrest John Pym, John Hampden, Denzil Holles, Arthur Haselrig and William Strode, five Members of his Parliament on the grounds that they had encouraged the Scots to invade England.
William Strode was the son of William Strode of Plympton in Devon, he married into the Meavy family of Meavy, eventually owning their estates in Devon.
The painting below, by Charles West Cope, shows the attempted arrest, it can be seen in the Houses of Parliament.
History is so interesting isn't it? Do you love the story of King Alfred's unsuccessful afternoon in the kitchen or King Cnut unsuccessful attempt not to get his feet wet? Maybe you're interested in when the Normans landing on our shores or the stories of an era closer to our time?
February 2020

subset: commoncrawl


text:
Gas tax money to be pumped into budget: Majority of $6.8M in road projects on east side
HILO — Some $6.8 million in new fuel tax money barely survived a close County Council vote last month, but its future seems more assured now that the Department of Public Works has released a working list of resurfacing projects to be completed with the money.
The council is set to cast its final vote Wednesday on Bill 211, which puts the money into the budget so the administration can spend it. The bill passed its first reading Dec. 19 by a 6-3 vote, the minimum number of yes votes required as spending bills require a two-thirds majority.
Voting no along with Kohala Councilman Tim Richards were newly elected Puna council members Matt Kanealii-Kleinfelder and Ashley Kierkiewicz.
Richards has been asking for months for a list of projects as required by the 2017 resolution that raised the tax. He was assured at a committee hearing Nov. 19 the list was forthcoming. But he didn't get the list until the day after his Dec. 19 negative vote.
"We had this in committee, we were promised a list of the roads that were going to be worked on in our districts. And they said we'd have it in a couple, three or four weeks, and it's a couple, three or four weeks and I'm wondering where our list is," Richards said during the council meeting. "I'm waiting for my list."
No one from Public Works was at the council meeting, but Finance Director Deanna Sako said a list does exist.
"I know they are working on it and they do have a list that they're working off of," Sako said. "I know they have a list and I'll remind them to get that to you guys right away."
Richards said through a council aide Thursday he received the list "timely," the day after the meeting.
Public Works Deputy Director Merrick Nishimoto, providing the list to the newspaper Thursday, said it's a work in progress and the department is refining its process to update the lists in a manner more compatible with those done by the state Department of Transportation.
"It's going to be less subjective," Nishimoto said. "We're doing a rating system so we compare it with the state as well, apples to apples."
Tops on the priority list, after completion of earlier priorities, are two Hamakua projects: No. 7, Kukuihaele, and No. 8, Old Mamalahoa (Ahualoa). The Old Mamalahoa Highway project commenced May 3, according to the list.
Pahoa Post Office Road, priority No. 10, is expected to start in April. It's not known when priority No. 11, South Point Road, will begin. Also in Ka'u, Wakea Avenue, priority No. 12, is expected to begin in the first quarter of this year.
Three resurfacing projects, Nos. 13-15 on the list, have already commenced. No. 13, Mamalahoa Highway in Captain Cook, fronting the fire station, began in December, while No. 14, the worst areas of Mamalahoa Highway from Teshima's to Haukapili in North Kona, and No. 15, Kamehameha from Waianuenue to Ponahawai in Hilo, began in November.
The road money is distributed based on the percentage of county roads in each district.
Of the $6.8 million collected, $3.4 million is slated for local road improvements, $2 million for engineering and $1.4 million for engineering and inspection of bridges.
The County Council in 2017 raised the county fuel tax from 8.8 cents per gallon to 15 cents, with an additional 4-cent increase last year and another 4-cent hike coming July 1, bringing the total to 23 cents per gallon this year.
The 2017 council measure establishing the fuel tax made the increase contingent on "the timely submission of a comprehensive plan by the Department of Public Works in collaboration with the Office of the Mayor providing the following minimum information: amount to be generated by increases; information on how money will be distributed to all districts; transportation projects to be funded in each district; and time-lines for projects utilizing fuel tax revenues."
Once again, no plan and a last minute submittal of bullsh*t projects that will never get done.
It's amazing that DPW failed to schedule any badly needed repairs of Hina Lani — one of West Hawaii's major (and well-traveled) few connector roads between Mamalahoa highway and Queen K highway, and Kona commerce centers.
Wagon trail-like road ruts of extended wear and tear now make navigation of the road unsafe, as on-coming trucks and cars play chicken to avoid the deteriorating bi-directional road conditions. DPW has allowed Hina Lani in large areas to simple break up and nearly return to a gravel base, all of which adds to taxpayer funded repair costs due to the agency's neglect and setting spending priorities for essential road maintenance.
The politics of setting east vs. west island resource priorities and the allocation of tax dollars is an old story, but common sense should dictate that Hini Lani is a road that deserves the County's immediate repair attention.
What a surprise.. the massive tax increases provided no real benefit.
So our benefit will be the paving of 6 miles for 6 million dollars in Hilo!
Headline should read. Gas tax money pumped into Harry $kims greedy pockets.


text:
Transplant Infections pp 599-608 | Cite as
Rhinovirus, Coronavirus, Enterovirus, and Bocavirus After Hematopoietic Cell Transplantation or Solid Organ Transplantation
- 1.7k Downloads
Respiratory viral infections represent a significant cause of morbidity and mortality in immunocompromised hosts. Newer molecular detection assays have allowed for the characterization of several respiratory viruses not previously recognized as having significant clinical impact in the immunocompromised population. Human rhinoviruses are the most common respiratory viruses detected in the upper respiratory tract of hematopoietic cell transplant and lung transplant recipients, and evidence on the impact on clinical outcomes is mounting. Other respiratory viruses including enteroviruses (EVs), coronaviruses (CoVs), and bocavirus may also contribute to pulmonary disease; however, data is limited in the immunocompromised population. Further studies are needed to define the epidemiology, risk factors, and clinical outcomes of these infections; this data will help inform decisions regarding development of antiviral therapy and infection prevention strategies.
KeywordsRhinovirus Enterovirus Coronavirus Bocavirus
32.1 Rhinoviruses
32.1.1 Epidemiology
Summary of clinical manifestations of rhinoviruses, coronaviruses, enteroviruses, and bocavirus
Upper respiratory tract infection
Lower respiratory tract infection
Other manifestations
Human rhinovirus
Supportive care
May be associated with severe disease in immunocompromised hosts
Gastrointestinal disease in children
Supportive care
Recent outbreaks of severe acute respiratory syndrome (SARS) and middle east respiratory syndrome (MERS)
Neurologic disease (poliomyelitis, meningitis, encephalitis), cardiac disease, muscle disease, eye infections
Supportive care
Sporadic outbreaks described, including Enterovirus-D68
Supportive care
HRVs are members of the Picornaviridae family and are classified into three species, HRV-A, HRV-B, and HRV-C, based on similarity in genome organization, capsid features, and conserved sequences [10]. The total number of genotypes continues to grow as new genotypes are characterized; currently at least 160 unique genotypes are described. Due to poor growth in traditional viral culture models, HRV-C was only recognized after the development of molecular diagnostic techniques. Thus, HRV-C is not a novel species, but rather one that has been circulating unnoticed due to lack of an appropriate diagnostic assay. There are several biologic characteristics of HRV-C that differentiate the species from HRV-A and HRV-B. HRV-A and HRV-B both use ICAM-1 or LDLR for cell attachment and entry, whereas it appears that HRV-C may utilize a distinct receptor, cadherin-related family member 3, that is associated with asthma susceptibility [11, 12]. Additionally, HRV-C species are stable at higher temperatures and readily infect upper and lower airways, whereas HRV-A and HRV-B species tend to be more limited to the sinuses and upper airways [13, 14]. These biologic characteristics are thought to play a role in variations in clinical outcomes observed among the different species.
32.1.2 Clinical Characteristics
Most immunocompetent patients with HRV present with an afebrile, self-limited syndrome characterized by rhinorrhea, nasal congestion, and malaise, and less frequently sore throat, mild cough, and hoarseness [15, 16, 17, 18, 19]. HRV may also be associated with exacerbations of sinusitis, chronic bronchitis, and asthma, and with lower respiratory tract syndromes and atypical pneumonias in otherwise healthy people, including the young and the elderly [20, 21]. The specific mechanisms by which HRVs produce lung diseases are not well understood. HRVs are also implicated in asthma and chronic obstructive pulmonary disease (COPD) exacerbations, but again the mechanisms are poorly defined.
With the widespread availability of PCR diagnostics, data are emerging on the incidence and clinical relevance of HRV infections in immunocompromised patients. Early studies relied on culture to detect HRV, a specific but insensitive method because the standard viral culture systems are not optimized for HRV detection, especially HRV-C [22]. For example, a Fred Hutchinson Cancer Center surveillance study from 1987 to 1992 detected HRVs in 29 specimens, and only one was from a lower respiratory tract specimen [2]. A prospective 5-year study at MD Anderson Cancer Center cultured specimens specifically for HRVs at lower temperatures with roller culture methods, and reported that HRV infections were associated with substantial morbidity and mortality in 7 of 22 (32%) myelosuppressed patients [23]. In that study, approximately one third of the adult HCT recipients who developed symptomatic HRV infections prior to engraftment had progression of upper respiratory tract symptoms to LRTI, and all cases with pneumonias were fatal. Lung biopsies and autopsies revealed findings consistent with interstitial pneumonitis and/or ARDS, but no in situ evaluation was performed to definitively assess HRV infection. Similar reports with evidence of LRTI based on radiographic and BAL findings continue to be noted [24, 25, 26], but it remains unknown if pneumonia is a direct cause of viral invasion of the lung tissue or by host responses in the lung. Evidence for in vitro and in vivo replication in lower respiratory tract has been shown in experimental infection, where HRV was isolated from human volunteers after intranasal HRV challenge by in situ hybridization [27]. The use of RT-PCR continues to provide new information about the frequency of HRV infection. In a study of BAL samples from 77 HCT recipients that were tested using RT-PCR , HRV was detected in six patients (8%), mortality rate was very high (83%) and two of the six patients showed persistent HRV infection. However, all of the HRV-infected patients had significant coinfections and it was not certain whether HRV infection was the direct cause of poor prognosis [25]. In a small cohort of patients with hematologic malignancy, LRTI was associated with hypoalbuminemia and bacterial co-pathogens were seen in 25% of patients [28].
Recent studies have shown that immunocompromised adults with HRV demonstrated similar hospital admission rates, intensive care unit admissions, and mortality rates as patients with pandemic H1N1 influenza [29]. Several reports have linked HRV infection to severe respiratory failure and even death [23, 24, 25]. Furthermore, recently presented data suggest that LRTI associated with HRV leads to a mortality rate comparable to that of RSV, influenza virus, and PIV [30], independent of the presence of co-pathogens. Risk factors for mortality following HRV LRTI included bone marrow stem cell source, oxygen requirement at time of diagnosis, and steroid use ≥1 mg/kg prior to diagnosis [30]. Other factors that may influence clinical severity include the presence of HRV RNA in blood, viral load, and HRV species type; however, no data exist in immunocompromised patients to date. HRV viral RNA was detected in the sera of 30 (12%) of 243 pediatric patients with severe HRV respiratory infection, with HRV-C being the predominant species [31]. In healthy pediatric patients, increased respiratory viral load has been associated with HRV LRTI and HRVC has been implicated as a more virulent pathogen [32, 33, 34]. Others, however, have shown lack of correlation between HRV-C and oxygen requirement, length of hospitalizations, and coinfections [35]. The predominance of HRV-C in HCT recipients has also been described in small studies, with higher rates of pneumonia in patients with HRV-C detected from the upper respiratory tract [36]. In a small cohort of patients with hematologic malignancies, the rate of LRTI was not different between patients infected with HRV-A, HRV-B, or HRV-C [28]. The relative risk of HRV-C infection in the immunocompromised population remains unknown, and more research is needed to define the role of strain differences on outcomes.
Detection and diagnosis of respiratory viral infections prior to transplant is a common clinical concern that has until recently only been evaluated in small cohorts for certain viruses [37, 38, 39, 40]. In a large, prospective surveillance cohort of allogeneic HCT recipients, detection of HRV pretransplant was associated with significantly fewer days alive and out of the hospital, and significantly higher mortality at 100 days posttransplant [41]. Further, larger prospective studies are needed to determine risk factors for posttransplant complications, the role of viral load and symptom burden at the time of transplantation, and the need to potentially delay transplantation for patients with HRV present prior to transplantation. Ultimately, the issue of viral causality of disease and evaluation of prophylactic and treatment modalities will need to be addressed. The impact of HRV infection prior to SOT is not known.
Like HCT recipients, SOT recipients are exposed to highly immunosuppressive regimens that leave them susceptible to respiratory viral infections. Lung transplant recipients have the added disadvantage of altered lung immunity due to factors such as impaired ciliary clearance, poor cough reflex, and abnormal lymphatic drainage. These factors can predispose to lower respiratory tract infections. The impact of HRV on outcomes in lung transplant recipients can range from asymptomatic infection to severe disease. In a pooled analysis of all respiratory viruses detected in lung transplant recipients, viruses were detected five times more frequently when respiratory symptoms were present [42]. A correlation between higher symptom scores and higher rhinovirus load in the upper respiratory tract has been demonstrated, although even asymptomatic patients can have relatively high viral loads [43]. The relative rate of progression from upper to lower tract disease for HRV specifically is not known, although the effect on lung function has been evaluated in aggregate for all respiratory viruses and suggests a decline in forced expiratory volume (FEV1) of −5% to −30% [42]. For HRV specifically, the FEV1 loss was similar to that seen in other respiratory viruses [8]. The correlation between respiratory viral infections and acute rejection, chronic rejection, and bronchiolitis obliterans syndrome (BOS) remains somewhat unclear, with several conflicting findings when respiratory viruses were evaluated in aggregate [6, 7, 8]. A recent large cohort of 250 lung transplant recipients, however, showed an independent association between respiratory viral infections (34% HRV) and chronic lung allograft dysfunction in multivariate models [9]. This association was influenced by time, with more of an effect within a shorter period following respiratory infection. Larger, prospective studies investing individual viruses are needed to clearly assess the impact on these outcomes.
32.1.3 Diagnosis
Unlike paramyxoviruses, HRV infection cannot be diagnosed based on characteristic histopathologic changes or changes in cell morphology. In the past, cell culture was used to diagnose HRV infection using multiple cell lines at low temperatures of 33–34 °C, often in rolling tubes. The cell lines utilized for the detection of HRVs may detect enteroviruses; HRV isolates are distinguished from enteroviruses by their lability in acid (loss in viral titer following exposure to a pH of 5). There are no commercially available antigen-detection assays or simple kits for the detection of HRV.
RT-PCR has dramatically improved the ability to both detect and characterize HRVs, with current assays at least two to three times more sensitive than conventional culture methods [44]. Some PCR assays are able to distinguish between enteroviruses and HRVs instead of the acid lability assays [45]. Typing of HRVs based on PCR amplification sequence variations in 5′-noncoding region also has been described [46]. New standardized methods to detect more of the over 100 strains of HRV have now been described [47]; however, commercially available multiplex respiratory viral PCR panels contain primer/probe sets that can cross-react between enterovirus and HRV strains. New strains and types of HRV are being detected frequently and more diseases associated with HRV are being described using new and diverse molecular methods.
32.1.4 Treatment Options
There are no approved antivirals for the treatment of HRV infections. Several agents have been evaluated in preclinical and clinical trials for the treatment of HRV infection in immunocompetent hosts, including capsid binding inhibitors, protease inhibitors, and RNA synthesis inhibitors [48]. None of these agents have been evaluated in immunocompromised hosts. Given the high prevalence and potential severity of HRV infection in this population, there is a great need for drug development and clinical trials for the prevention and treatment of LRTI. Outside of transplant recipients, there is a potential need for intervention in other populations such as patients with asthma or COPD to prevent disease exacerbation [49, 50].
32.2 Coronaviruses
32.2.1 Epidemiology
CoVs are a frequent cause of the common cold, but little is known about the role of CoVs in immunocompromised patients [51] (Table 32-1). Human group 1 (subtypes 229E and NL63) and human group 2 (OC43 and HKU1) CoVs were originally reported as causes of human respiratory illnesses. The availability of more sophisticated diagnostic tools, such as RT-PCR , has facilitated the detection of CoVs in normal and immunocompromised persons. These improved molecular methods of viral discovery facilitated the recent identification of the novel Group 1 and 2 human CoV subtypes—NL63 in 2004 [52] and HKU1 in 2005 [53]. A more accurate clinical epidemiology of CoV infection is beginning to emerge. It is now known that all four known subtypes of CoV circulate simultaneously [54], and that in addition to the common cold, CoV is associated with upper respiratory tract infection and LRTI in persons with and without underlying conditions [55, 56]. In lung transplant recipients, CoVs appear to be the second most common respiratory viruses after picornaviruses with a detection rate of 13–27% of positive samples [5, 6, 7] (Figure 32-2). In a prospective surveillance cohort of lung transplant recipients, coronaviruses were detected in 13% of all positive samples, again only second to picornaviruses [8].
Two additional CoVs associated with outbreaks are the severe acute respiratory syndrome-associated CoV (SARS-CoV) and the recently described Middle East respiratory syndrome-CoV (MERS-CoV). The SARS outbreak originated in Guangdong Province in China in 2002 and was characterized by a life-threatening, atypical pneumonia and was spread by close contact with infected humans, mostly to household contacts and health care workers [57]. SARS-CoV is not currently circulating in the world with the most recent human cases of infection reported in China in 2004 [58]. MERS-CoV first emerged in the Arabian Peninsula in 2012, and since then travel-associated cases have been found in a number of countries outside the region [59]. In adults, the fatality rate is estimated to be 40%; in children asymptomatic infection is common but patients with underlying medical conditions are at increased risk [60, 61]. There is little data on the incidence of SARS-CoV and MERS-CoV in immunocompromised hosts, although immune suppression is considered a risk factor. SARS-CoV has been described in liver transplant recipients and in patients with myelodysplastic syndrome [62, 63]. MERS-CoV has been described in patients on chronic immunosuppression and in renal transplant recipients with a broad range of clinical presentations [64, 65]. Other CoVs have been reported to cause pneumonia in children and immunocompromised patients treated for hematologic malignancies [66, 67, 68]. The role of coronavirus virus infection prior to transplantation is not known.
32.2.2 Clinical Characteristics
Although most CoV infections result in relatively mild upper respiratory tract infection, these viruses have been associated with more severe LRTI (e.g., bronchiolitis and pneumonia) in patients who are immunosuppressed, have asthma, or are premature. In one retrospective study carried out over 1 year, CoV was detected in six immunocompromised children—five with acute lymphocytic leukemia and one renal transplant recipient [54]. Five patients were febrile at the time coronavirus was present, with fevers lasting 1–7 days. All patients initially presented with rhinorrhea and nasal discharge; two children had cough as a presenting symptom. Chest radiographs of only one of the three children were abnormal; LRTI based on decreased oxygen saturation, tachypnea, and abnormal chest radiograph was present in only one child with leukemia, who was significantly neutropenic and lymphopenic at the time CoV was detected. CoVs have been associated with LRTI in HCT recipients with sometimes fatal outcomes [66, 67, 69, 70, 71]. The clinical characteristics of SARS-CoV and MERS-CoV infection in HCT and SOT patients are not well described, and presentation can range from mild symptoms to respiratory failure and death [62, 63, 64, 65, 72].
32.2.3 Diagnosis
Until the advent of RT-PCR , techniques for the detection of CoV were limited and the reliable identification of CoV was problematic. Early detection techniques isolated two subtypes—OC43 and 229E, originally using organ cultures of human embryonic trachea, with morphology determined using negative staining with electron microscopy [73]. With the advent of molecular detection methods and increased interest in CoV detection during the SARS outbreak, new strains of CoVs have been discovered and new RT-PCR assays developed that facilitate further studies of these viruses. Based on RT-PCR assays, four strains of non-SARS CoVs (OC43, 229E, NL63, and HKU1) appear to cocirculate during the non-summer months in temperate climates, and are associated with symptomatic disease in immunocompromised hosts [54]. Guidance on RT-PCR and serologic assays for the confirmation on MERS-CoV can be found on the World Health Organization website [74].
32.2.4 Treatment Options
There are no approved antivirals for prophylaxis or treatment of CoV infections and supportive care remains paramount in managing patients infected with coronaviruses. Though several antivirals were used during the SARS-CoV epidemic, no clear benefit could be established on systematic review [75]. Oral ribavirin was evaluated in retrospective studies for the treatment of MERS-CoV in immunocompetent individuals; decreased survival was noted in one study when compared to matched controls [76, 77], however, larger prospective studies are needed to show true efficacy. Shedding of all coronaviruses may persist for up to months, and routine infection control practices are encouraged.
32.3 Enteroviruses
32.3.1 Epidemiology
EVs are part of the picornaviridae family of viruses and can be associated with severe illness in immunocompromised hosts. EVs include polioviruses, coxsackieviruses, and echoviruses; these are now all classified into four species: Enterovirus A (EV-A), EV-B, EV-C, and EV-D. Risk for infection and subsequent poor outcomes appears to be heavily influenced by age, although factors such as sex and socioeconomic status play a role in the general population. EV activity can be either sporadic or epidemic, and several outbreaks have been described. EVs are typically found during the summer and early autumn in temperate climates.
Enterovirus-D68 (EV-D68) was first identified in California in 1962 [78] and has since been associated with several small outbreaks, both in the US and internationally, from 2009 to 2013 [79, 80, 81, 82, 83, 84]. In the summer of 2014, several hundred cases of severe respiratory illnesses in children in the United States were found to be associated with EV-D68 infection [85], and several additional clusters have been described worldwide [86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96].
32.3.2 Clinical Characteristics
EVs can cause a wide spectrum of illnesses in immunocompetent individuals including asymptomatic infection, poliomyelitis, meningitis, encephalitis, cardiac disease, muscle disease, eye infections, respiratory infections, exanthems, and neonatal disease. The most frequently described manifestation in immunocompromised patients is respiratory disease, although the incidence and spectrum of disease is not known. According to one study, EVs can be associated with lower respiratory tract infection and mortality; however, larger studies are needed to establish specific risk factors for worse outcomes [97].
Most confirmed cases of EV-D68 infection have been in children, occurring primarily in patients with underlying lung disease such as asthma or a history of wheezing. EV-D68 was also associated with several cases of acute flaccid paralysis in children during the 2014 outbreak in the United States, although definitive causation has not yet been established [98, 99]. The impact of EV-D68 infection in immunocompromised hosts is not known; however, the association between EV-D68 and severe illness was described in eight adult immunocompromised patients with presumptive EV-D68 infection including HCT recipients [100]. Additionally, one recent report of adults with confirmed EV-D68 infection included solid organ transplant recipients [87].
32.3.3 Diagnosis
Depending on the clinical scenario, EVs can be detected from a number of clinical specimens including cerebral spinal fluid, serum, respiratory specimens, cardiac tissue, and stool. EVs may be identified in throat samples as well as fecal specimens and cerebrospinal fluid. Commercial multiplex PCR assays contain primer/probe sets that may cross react between rhinoviruses and enteroviruses. A specific EV-D68 RT-PCR has been developed by the CDC and has been made publically available [101].
32.3.4 Treatment Options
There are no approved antivirals approved for the treatment of EVs. Intravenous immunoglobulin (IVIG) has been used in the treatment of neonatal enteroviral sepsis, but the effect on clinical outcomes is highly dependent on the presence of specific neutralizing antibodies and timing of administration [102, 103]. Pleconaril, an oral capsid inhibitor with activity against picornaviruses, has been evaluated in treatment of enteroviral infections including meningitis, neonatal sepsis, and respiratory infections [104, 105, 106, 107, 108] but is not available for treatment. Other capsid binders, protease inhibitors, and polymerase inhibitors are in various stages of development, but none are currently available for treatment of enteroviral infections [109]. No studies have shown efficacy in immunocompromised hosts.
32.4 Bocavirus
Human bocavirus (HBoV) is a newly identified human parvovirus that was originally identified by random PCR amplification/cloning technique on pooled respiratory secretions from hospitalized children with respiratory tract symptoms [110]. This virus was named "human bocavirus," due to its relatedness to the genome organization of two other parvoviruses, bovine parvovirus and minute virus of canines, in the family Parvoviridae. This virus continues to be detected in young children with a winter seasonality [111, 112, 113]. The relationship of HBoV and respiratory disease in immunocompromised patients is not yet clear. Preliminary evidence to date demonstrates case reports of disseminated HBoV infection with involvement of the respiratory tract, blood, and stool in several patients, sometimes associated with GVHD and prolonged viral shedding in the feces [114, 115]. Other studies have reported little evidence linking this virus with pulmonary pathology or severe respiratory disease in HCT or lung transplant recipients [116, 117, 118]. Further research is necessary to link this virus with the disease in the transplant recipient. No specific antiviral therapy is available.
32.5 Future Directions and Unmet Needs
Respiratory viruses are a significant concern following HCT and SOT and can be associated with substantial morbidity and mortality, even among viruses traditionally not concerned pathogenic. New, sensitive diagnostic assays allow for routine detection of rhinoviruses, enteroviruses, coronaviruses, and bocavirus, and additional data on the epidemiology, risk factors, outcomes of infection, and the impact of different viral strains are desperately needed. Preliminary studies suggest that detection of these viruses prior to transplant may affect outcomes, but additional studies are needed to explore this important clinical area. Furthermore, as new antivirals are being developed, it will be important to identify high-risk patients that may benefit from treatment. Finally, a better understanding of these viruses will be able to inform better infection prevention strategies that will remain the mainstay of viral control.
- 1.Ljungman P, Ward KN, Crooks BNA, Parker A, Martino R, Shaw PJ, et al. Respiratory virus infections after stem cell transplantation: a prospective study from the Infectious Diseases Working Party of the European Group for Blood and Marrow Transplantation. Bone Marrow Transplant. 2001;28(5):479–84.PubMedCrossRefGoogle Scholar
- 2.Bowden MDRA. Respiratory virus infections after marrow transplant: the Fred Hutchinson cancer research center experience. Am J Med. 1997;102(3):27–30.PubMedCrossRefGoogle Scholar
- 3.Hassan IA, Chopra R, Swindell R, Mutton KJ. Respiratory viral infections after bone marrow/peripheral stem-cell transplantation: the Christie hospital experience. Bone Marrow Transplant. 2003;32(1):73–7.PubMedCrossRefGoogle Scholar
- 4.Milano F, Campbell AP, Guthrie KA, Kuypers J, Englund JA, Corey L, et al. Human rhinovirus and coronavirus detection among allogeneic hematopoietic stem cell transplantation recipients. Blood. 2010;115(10):2088–94.PubMedPubMedCentralCrossRefGoogle Scholar
- 5.Kumar D, Erdman D, Keshavjee S, Peret T, Tellier R, Hadjiliadis D, et al. Clinical impact of community-acquired respiratory viruses on bronchiolitis obliterans after lung transplant. Am J Transplant. 2005;5(8):2031–6.PubMedCrossRefGoogle Scholar
- 6.Soccal PM, Aubert JD, Bridevaux PO, Garbino J, Thomas Y, Rochat T, et al. Upper and lower respiratory tract viral infections and acute graft rejection in lung transplant recipients. Clin Infect Dis. 2010;51(2):163–70.PubMedCrossRefGoogle Scholar
- 7.Kumar D, Husain S, Chen MH, Moussa G, Himsworth D, Manuel O, et al. A prospective molecular surveillance study evaluating the clinical impact of community-acquired respiratory viruses in lung transplant recipients. Transplantation. 2010;89(8):1028–33.PubMedCrossRefGoogle Scholar
- 8.Bridevaux PO, Aubert JD, Soccal PM, Mazza-Stalder J, Berutto C, Rochat T, et al. Incidence and outcomes of respiratory viral infections in lung transplant recipients: a prospective study. Thorax. 2014;69(1):32–8.PubMedCrossRefGoogle Scholar
- 9.Fisher CE, Preiksaitis CM, Lease ED, Edelman J, Kirby KA, Leisenring WM, Boeckh M, Limaye AP. Symptomatic respiratory virus infection and chronic lung allograft dysfunction. Clin Infect Dis. 2016;62(3):313–9.PubMedCrossRefGoogle Scholar
- 10.Palmenberg AC, Rathe JA, Liggett SB. Analysis of the complete genome sequences of human rhinovirus. J Allergy Clin Immunol. 2010;125(6):1190–9. quiz 200–1.PubMedPubMedCentralCrossRefGoogle Scholar
- 11.Vlasak M, Roivainen M, Reithmayer M, Goesler I, Laine P, Snyers L, et al. The minor receptor group of human rhinovirus (HRV) includes HRV23 and HRV25, but the presence of a lysine in the VP1 HI loop is not sufficient for receptor binding. J Virol. 2005;79(12):7389–95.PubMedPubMedCentralCrossRefGoogle Scholar
- 12.Bochkov YA, Watters K, Ashraf S, Griggs TF, Devries MK, Jackson DJ, et al. Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication. Proc Natl Acad Sci U S A. 2015;112(17):5485–90.PubMedPubMedCentralCrossRefGoogle Scholar
- 13.Bochkov YA, Gern JE. Clinical and molecular features of human rhinovirus C. Microbes Infect. 2012;14(6):485–94.PubMedPubMedCentralCrossRefGoogle Scholar
- 14.Ashraf S, Brockman-Schneider R, Bochkov YA, Pasic TR, Gern JE. Biological characteristics and propagation of human rhinovirus-C in differentiated sinus epithelial cells. Virology. 2013;436(1):143–9.PubMedCrossRefGoogle Scholar
- 15.Arruda E, Pitkaranta A, Witek Jr TJ, Doyle CA, Hayden FG. Frequency and natural history of rhinovirus infections in adults during autumn. J Clin Microbiol. 1997;35(11):2864–8.PubMedPubMedCentralGoogle Scholar
- 16.Johnston SL. Natural and experimental rhinovirus infections of the lower respiratory tract. Am J Respir Crit Care Med. 1995;152(4 pt 2):S46–52.PubMedCrossRefGoogle Scholar
- 17.Gern JE, Palmenberg AC. Rhinoviruses. In: Knipe DM, Howley PM, editors. Fields virology. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. p. 531–49.Google Scholar
- 18.Couch MDRB, Englund MDJA. Respiratory viral infections in immunocompetent and immunocompromised persons. Am J Med. 1997;102(3):2–9.PubMedCrossRefGoogle Scholar
- 19.Gwaltney J, Rueckert R. Rhinovirus. In: Richman DD, Whitley RJ, Hayden FG, editors. Clinical virology. New York: Churchill Livingstone; 1997. p. 1025–47.Google Scholar
- 20.Gern JE, Galagan DM, Jarjour NN, Dick EC, Busse WW. Detection of rhinovirus RNA in lower airway cells during experimentally induced infection. Am J Respir Crit Care Med. 1997;155(3):1159–61.PubMedCrossRefGoogle Scholar
- 21.Jain S, Self WH, Wunderink RG, Fakhran S, Balk R, Bramley AM, et al. Community-acquired pneumonia requiring hospitalization among U.S. adults. N Engl J Med. 2015;373(5): 415–27.PubMedPubMedCentralCrossRefGoogle Scholar
- 22.Landry M. Rhinoviruses. In: Versalovic J, Carroll KC, Funke G, Jorgensen JH, Landry ML, Warnock DW, editors. Manual of clinical microbiology. 10th ed. Washington, DC: ASM Press; 2011. p. 1400–9.Google Scholar
- 23.Ghosh S, Champlin R, Couch R, Englund J, Malik S. Rhinovirus infections in myelosuppressed adult blood and marrow transplant recipients. Clin Infect Dis. 1999;29(3):528–32.PubMedCrossRefGoogle Scholar
- 24.Gutman JA, Peck AJ, Kuypers J, Boeckh M. Rhinovirus as a cause of fatal lower respiratory tract infection in adult stem cell transplantation patients: a report of two cases. Bone Marrow Transplant. 2007;40(8):809–11.PubMedCrossRefGoogle Scholar
- 25.Ison MG, Hayden FG, Kaiser L, Corey L, Boeckh M. Rhinovirus infections in hematopoietic stem cell transplant recipients with pneumonia. Clin Infect Dis. 2003;36(9):1139–43.PubMedCrossRefGoogle Scholar
- 26.Jacobs SE, Soave R, Shore TB, Satlin MJ, Schuetz AN, Magro C, et al. Human rhinovirus infections of the lower respiratory tract in hematopoietic stem cell transplant recipients. Transpl Infect Dis. 2013;15(5):474–86.PubMedPubMedCentralGoogle Scholar
- 27.Papadopoulos Nikolaos G, Bates Philip J, Bardin Philip G, Papi A, Leir Shih H, Fraenkel David J, et al. Rhinoviruses infect the lower airways. J Infect Dis. 2000;181(6):1875–84.CrossRefGoogle Scholar
- 28.Jacobs SE, Lamson DM, Soave R, Guzman BH, Shore TB, Ritchie EK, et al. Clinical and molecular epidemiology of human rhinovirus infections in patients with hematologic malignancy. J Clin Virol. 2015;71:51–8.PubMedPubMedCentralCrossRefGoogle Scholar
- 29.Kraft CS, Jacob JT, Sears MH, Burd EM, Caliendo AM, Lyon GM. Severity of human rhinovirus infection in immunocompromised adults is similar to that of 2009 H1N1 influenza. J Clin Microbiol. 2012;50(3):1061–3.PubMedPubMedCentralCrossRefGoogle Scholar
- 30.Seo S, Martin E, Xie H, Kuypers J, Campbell AP, Choi S, Waghmare A, Leisenring W, Jerome K, Englund J, Boeckh. Human Rhinovirus RNA Detection in the Lower Respiratory Tract of Hematopoietic Cell Transplant recipients: Association with Mortality. Abstract presented at: ASBMT Tandem Meeting; 2013;13–17; Salt Lake City, UT.Google Scholar
- 31.Fuji N, Suzuki A, Lupisan S, Sombrero L, Galang H, Kamigaki T, et al. Detection of human rhinovirus C viral genome in blood among children with severe respiratory infections in the Philippines. PLoS One. 2011;6(11):e27247.PubMedPubMedCentralCrossRefGoogle Scholar
- 32.Martin EK, Kuypers J, Chu HY, Lacombe K, Qin X, Strelitz B, et al. Molecular epidemiology of human rhinovirus infections in the pediatric emergency department. J Clin Virol. 2015;62:25–31.PubMedCrossRefGoogle Scholar
- 33.Bizzintino J, Lee WM, Laing IA, Vang F, Pappas T, Zhang G, et al. Association between human rhinovirus C and severity of acute asthma in children. Eur Respir J. 2011;37(5):1037–42.PubMedCrossRefGoogle Scholar
- 34.Takeyama A, Hashimoto K, Sato M, Sato T, Kanno S, Takano K, et al. Rhinovirus load and disease severity in children with lower respiratory tract infections. J Med Virol. 2012;84(7):1135–42.PubMedCrossRefGoogle Scholar
- 35.Launes C, Armero G, Anton A, Hernandez L, Gimferrer L, Cisneros C, et al. Molecular epidemiology of severe respiratory disease by human rhinoviruses and enteroviruses at a tertiary paediatric hospital in Barcelona, Spain. Clin Microbiol Infect. 2015;21(8):799.e5–7.Google Scholar
- 36.Ferguson PE, Gilroy NM, Faux CE, Mackay IM, Sloots TP, Nissen MD, et al. Human rhinovirus C in adult haematopoietic stem cell transplant recipients with respiratory illness. J Clin Virol. 2013;56(3):255–9.PubMedCrossRefGoogle Scholar
- 37.Peck AJ, Corey L, Boeckh M. Pretransplantation respiratory syncytial virus infection: impact of a strategy to delay transplantation. Clin Infect Dis. 2004;39(5):673–80.PubMedCrossRefGoogle Scholar
- 38.Ljungman P, Gleaves CA, Meyers JD. Respiratory virus infection in immunocompromised patients. Bone Marrow Transplant. 1989;4(1):35–40.PubMedGoogle Scholar
- 39.Bredius RG, Templeton KE, Scheltinga SA, Claas EC, Kroes AC, Vossen JM. Prospective study of respiratory viral infections in pediatric hemopoietic stem cell transplantation patients. Pediatr Infect Dis J. 2004;23(6):518–22.PubMedCrossRefGoogle Scholar
- 40.Templeton KE, Bredius RG, Scheltinga SA, Claas EC, Vossen JM, Kroes AC. Parainfluenza virus 3 infection pre- and post-haematopoietic stem cell transplantation: re-infection or persistence? J Clin Virol. 2004;29(4):320–2.PubMedCrossRefGoogle Scholar
- 41.Campbell AP, Guthrie KA, Englund JA, Farney RM, Minerich EL, Kuypers J, et al. Clinical outcomes associated with respiratory virus detection before allogeneic hematopoietic stem cell transplant. Clin Infect Dis. 2015;61(2):192–202.PubMedPubMedCentralCrossRefGoogle Scholar
- 42.Vu DL, Bridevaux PO, Aubert JD, Soccal PM, Kaiser L. Respiratory viruses in lung transplant recipients: a critical review and pooled analysis of clinical studies. Am J Transplant. 2011;11(5):1071–8.PubMedCrossRefGoogle Scholar
- 43.Ambrosioni J, Bridevaux PO, Aubert JD, Soccal P, Wagner G, Kaiser L. Role of rhinovirus load in the upper respiratory tract and severity of symptoms in lung transplant recipients. J Clin Virol. 2015;64:1–5.PubMedCrossRefGoogle Scholar
- 44.Johnston SL, Sanderson G, Pattemore PK, Smith S, Bardin PG, Bruce CB, et al. Use of polymerase chain reaction for diagnosis of picornavirus infection in subjects with and without respiratory symptoms. J Clin Microbiol. 1993;31(1):111–7.PubMedPubMedCentralGoogle Scholar
- 45.Atmar RL, Georghiou PR. Classification of respiratory tract picornavirus isolates as enteroviruses or rhinoviruses by using reverse transcription-polymerase chain reaction. J Clin Microbiol. 1993;31(9):2544–6.PubMedPubMedCentralGoogle Scholar
- 46.Torgersen H, Skern T, Blaas D. Typing of human rhinoviruses based on sequence variations in the 5′ non-coding region. J Gen Virol. 1989;70(11):3111–6.PubMedCrossRefGoogle Scholar
- 47.Lu X, Holloway B, Dare RK, Kuypers J, Yagi S, Williams JV, et al. Real-time reverse transcription-PCR assay for comprehensive detection of human rhinoviruses. J Clin Microbiol. 2007;46(2):533–9.PubMedPubMedCentralCrossRefGoogle Scholar
- 48.Rollinger JM, Schmidtke M. The human rhinovirus: human-pathological impact, mechanisms of antirhinoviral agents, and strategies for their discovery. Med Res Rev. 2011;31(1):42–92.PubMedCrossRefGoogle Scholar
- 49.Thibaut HJ, Lacroix C, De Palma AM, Franco D, Decramer M, Neyts J. Toward antiviral therapy/prophylaxis for rhinovirus-induced exacerbations of chronic obstructive pulmonary disease: challenges, opportunities, and strategies. Rev Med Virol. 2015. doi: 10.1002/rmv.1856 [Epub ahead of print].
- 50.Hammond C, Kurten M, Kennedy JL. Rhinovirus and asthma: a storied history of incompatibility. Curr Allergy Asthma Rep. 2015;15(2):502.PubMedPubMedCentralCrossRefGoogle Scholar
- 51.McIntosh K. Coronaviruses. In: Richman D, Whitley RJ, Hayden FG, editors. Clinical virology. New York: Churchill Livingstone; 1997. p. 1123–32.Google Scholar
- 52.van der Hoek L, Pyrc K, Jebbink MF, Vermeulen-Oost W, Berkhout RJM, Wolthers KC, et al. Identification of a new human coronavirus. Nat Med. 2004;10(4):368–73.PubMedCrossRefGoogle Scholar
- 53.Woo PC, Lau SK, Chu CM, Chan KH, Tsoi HW, Huang Y, et al. Characterization and complete genome sequence of a novel coronavirus, coronavirus HKU1, from patients with pneumonia. J Virol. 2004;79(2):884–95.CrossRefGoogle Scholar
- 54.Kuypers J, Martin ET, Heugel J, Wright N, Morrow R, Englund JA. Clinical disease in children associated with newly described coronavirus subtypes. Pediatrics. 2007;119(1):e70–6.PubMedCrossRefGoogle Scholar
- 55.Heugel J, Martin ET, Kuypers J, Englund JA. Coronavirus-associated pneumonia in previously healthy children. Pediatr Infect Dis J. 2007;26(8):753–5.PubMedCrossRefGoogle Scholar
- 56.Lee J, Storch GA. Characterization of human coronavirus OC43 and human coronavirus NL63 infections among hospitalized children <5 years of age. Pediatr Infect Dis J. 2014;33(8):814–20.PubMedCrossRefGoogle Scholar
- 57.Shi Z, Hu Z. A review of studies on animal reservoirs of the SARS coronavirus. Virus Res. 2008;133(1):74–87.PubMedCrossRefGoogle Scholar
- 58.Liang WN, Zhao T, Liu ZJ, Guan BY, He X, Liu M, et al. Severe acute respiratory syndrome—retrospect and lessons of 2004 outbreak in China. Biomed Environ Sci. 2006;19(6):445–51.PubMedGoogle Scholar
- 59.Rha B, Rudd J, Feikin D, Watson J, Curns AT, Swerdlow DL, et al. Update on the epidemiology of Middle East respiratory syndrome coronavirus (MERS-CoV) infection, and guidance for the public, clinicians, and public health authorities. MMWR Morb Mortal Wkly Rep. 2015;64(3):61–2.PubMedPubMedCentralGoogle Scholar
- 60.Majumder MS, Rivers C, Lofgren E, Fisman D. Estimation of MERS-coronavirus reproductive number and case fatality rate for the Spring 2014 Saudi Arabia outbreak: insights from publicly available data. PLoS Curr. 2014;6.Google Scholar
- 61.Memish ZA, Al-Tawfiq JA, Assiri A, AlRabiah FA, Al Hajjar S, Albarrak A, et al. Middle east respiratory syndrome coronavirus disease in children. Pediatr Infect Dis J. 2014;33(9): 904–6.PubMedCrossRefGoogle Scholar
- 62.Kumar D, Tellier R, Draker R, Levy G, Humar A. Severe Acute Respiratory Syndrome (SARS) in a liver transplant recipient and guidelines for donor SARS screening. Am J Transplant. 2003;3(8):977–81.PubMedCrossRefGoogle Scholar
- 63.Lee N, Hui D, Wu A, Chan P, Cameron P, Joynt GM, et al. A major outbreak of severe acute respiratory syndrome in Hong Kong. N Engl J Med. 2003;348(20):1986–94.PubMedCrossRefGoogle Scholar
- 64.Guery B, Poissy J, el Mansouf L, Sejourne C, Ettahar N, Lemaire X, et al. Clinical features and viral diagnosis of two cases of infection with Middle East Respiratory Syndrome coronavirus: a report of nosocomial transmission. Lancet. 2013;381(9885):2265–72.PubMedCrossRefGoogle Scholar
- 65.AlGhamdi M, Mushtaq F, Awn N, Shalhoub S. MERS CoV infection in two renal transplant recipients: case report. Am J Transplant. 2015;15(4):1101–4.PubMedCrossRefGoogle Scholar
- 66.Oosterhof L, Christensen CB, Sengelov H. Fatal lower respiratory tract disease with human corona virus NL63 in an adult haematopoietic cell transplant recipient. Bone Marrow Transplant. 2010;45(6):1115–6.PubMedCrossRefGoogle Scholar
- 67.Pene F, Merlat A, Vabret A, Rozenberg F, Buzyn A, Dreyfus F, et al. Coronavirus 229E-related pneumonia in immunocompromised patients. Clin Infect Dis. 2003;37(7):929–32.PubMedCrossRefGoogle Scholar
- 68.Simon A, Volz S, Fleischhack G, Tillman R, Muller A, Bode U, et al. Human coronavirus OC43 pneumonia in a pediatric cancer patient with Down syndrome and acute lymphoblastic leukemia. J Pediatr Hematol Oncol. 2007;29(6):432–4.PubMedCrossRefGoogle Scholar
- 69.Gerna G, Campanini G, Rovida F, Percivalle E, Sarasini A, Marchi A, et al. Genetic variability of human coronavirus OC43-, 229E-, and NL63-like strains and their association with lower respiratory tract infections of hospitalized infants and immunocompromised patients. J Med Virol. 2006;78(7): 938–49.PubMedCrossRefGoogle Scholar
- 70.Folz RJ, Elkordy MA. Coronavirus pneumonia following autologous bone marrow transplantation for breast cancer. Chest. 1999;115(3):901–5.PubMedCrossRefGoogle Scholar
- 71.Uhlenhaut C, Cohen JI, Pavletic S, Illei G, Gea-Banacloche JC, Abu-Asab M, et al. Use of a novel virus detection assay to identify coronavirus HKU1 in the lungs of a hematopoietic stem cell transplant recipient with fatal pneumonia. Transpl Infect Dis. 2012;14(1):79–85.PubMedCrossRefGoogle Scholar
- 72.Gomersall CD, Joynt GM, Lam P, Li T, Yap F, Lam D, et al. Short-term outcome of critically ill patients with severe acute respiratory syndrome. Intensive Care Med. 2004;30(3):381–7.PubMedCrossRefGoogle Scholar
- 73.Monto AS. Coronaviruses. Viral infections of humans. New York: Springer; 1997. p. 211–27.CrossRefGoogle Scholar
- 74.World Health Organization. Laboratory testing for Middle East respiratory syndrome coronavirus 2015. Available from: http://www.who.int/csr/disease/coronavirus_infections/mers-laboratory-testing/en/.
- 75.Stockman LJ, Bellamy R, Garner P. SARS: systematic review of treatment effects. PLoS Med. 2006;3(9):e343.PubMedPubMedCentralCrossRefGoogle Scholar
- 76.Omrani AS, Saad MM, Baig K, Bahloul A, Abdul-Matin M, Alaidaroos AY, et al. Ribavirin and interferon alfa-2a for severe Middle East respiratory syndrome coronavirus infection: a retrospective cohort study. Lancet Infect Dis. 2014;14(11):1090–5.PubMedCrossRefGoogle Scholar
- 77.Al-Tawfiq JA, Momattin H, Dib J, Memish ZA. Ribavirin and interferon therapy in patients infected with the Middle East respiratory syndrome coronavirus: an observational study. Int J Infect Dis. 2014;20:42–6.PubMedCrossRefGoogle Scholar
- 78.Schieble JH, Fox VL, Lennette EH. A probable new human picornavirus associated with respiratory diseases. Am J Epidemiol. 1967;85(2):297–310.PubMedCrossRefGoogle Scholar
- 79.Centers for Disease Control and Prevention. Clusters of acute respiratory illness associated with human enterovirus 68—Asia, Europe, and United States, 2008–2010. MMWR Morb Mortal Wkly Rep. 2011;60(38):1301–4.Google Scholar
- 80.Imamura T, Fuji N, Suzuki A, Tamaki R, Saito M, Aniceto R, et al. Enterovirus 68 among children with severe acute respiratory infection, the Philippines. Emerg Infect Dis. 2011;17(8):1430–5.PubMedPubMedCentralGoogle Scholar
- 81.Imamura T, Suzuki A, Lupisan S, Kamigaki T, Okamoto M, Roy CN, et al. Detection of enterovirus 68 in serum from pediatric patients with pneumonia and their clinical outcomes. Influenza Other Respi Viruses. 2014;8(1):21–4.CrossRefGoogle Scholar
- 82.Kaida A, Kubo H, Sekiguchi J, Kohdera U, Togawa M, Shiomi M, et al. Enterovirus 68 in children with acute respiratory tract infections, Osaka, Japan. Emerg Infect Dis. 2011;17(8):1494–7.PubMedPubMedCentralGoogle Scholar
- 83.Wang YC, Cheng HB, Chen HH, Liu CM, Chou CH, Sung FC. Circulating viruses associated with severe complicated enterovirus infection in Taiwan: a multi-year analysis. Pediatr Infect Dis J. 2010;29(4):334–9.PubMedGoogle Scholar
- 84.Kreuter JD, Barnes A, McCarthy JE, Schwartzman JD, Oberste MS, Rhodes CH, et al. A fatal central nervous system enterovirus 68 infection. Arch Pathol Lab Med. 2011;135(6):793–6.PubMedGoogle Scholar
- 85.Midgley CM, Jackson MA, Selvarangan R, Turabelidze G, Obringer E, Johnson D, et al. Severe respiratory illness associated with enterovirus D68—Missouri and Illinois, 2014. MMWR Morb Mortal Wkly Rep. 2014;63(36):798–9.PubMedPubMedCentralGoogle Scholar
- 86.Bragstad K, Jakobsen K, Rojahn AE, Skram MK, Vainio K, Holberg-Petersen M, et al. High frequency of enterovirus D68 in children hospitalised with respiratory illness in Norway, autumn 2014. Influenza Other Respi Viruses. 2015;9(2):59–63.CrossRefGoogle Scholar
- 87.Poelman R, Scholvinck EH, Borger R, Niesters HG, van Leer-Buter C. The emergence of enterovirus D68 in a Dutch University Medical Center and the necessity for routinely screening for respiratory viruses. J Clin Virol. 2015;62:1–5.PubMedCrossRefGoogle Scholar
- 88.Furuse Y, Chaimongkol N, Okamoto M, Imamura T, Saito M, Tamaki R, et al. Molecular epidemiology of enterovirus d68 from 2013 to 2014 in Philippines. J Clin Microbiol. 2015;53(3):1015–8.PubMedPubMedCentralCrossRefGoogle Scholar
- 89.Drews SJ, Simmonds K, Usman HR, Yee K, Fathima S, Tipples G, et al. Characterization of enterovirus activity, including that of enterovirus D68, in pediatric patients in Alberta, Canada, in 2014. J Clin Microbiol. 2015;53(3):1042–5.PubMedPubMedCentralCrossRefGoogle Scholar
- 90.Vongpunsawad S, Prachayangprecha S, Chansaenroj J, Haagmans BL, Smits SL, Poovorawan Y. Genome sequence of enterovirus D68 and clinical disease, Thailand. Emerg Infect Dis. 2015;21(2):384.PubMedPubMedCentralCrossRefGoogle Scholar
- 91.Pfeiffer HC, Bragstad K, Skram MK, Dahl H, Knudsen PK, Chawla MS, et al. Two cases of acute severe flaccid myelitis associated with enterovirus D68 infection in children, Norway, autumn 2014. Euro Surveill. 2015;20(10):21062.PubMedCrossRefGoogle Scholar
- 92.Torres JP, Farfan MJ, Izquierdo G, Piemonte P, Henriquez J, O'Ryan ML. Enterovirus D68 infection, Chile, Spring 2014. Emerg Infect Dis. 2015;21(4):728–9.PubMedPubMedCentralCrossRefGoogle Scholar
- 93.Reiche J, Bottcher S, Diedrich S, Buchholz U, Buda S, Haas W, et al. Low-level circulation of enterovirus D68-associated acute respiratory infections, Germany, 2014. Emerg Infect Dis. 2015;21(5):837–41.PubMedPubMedCentralCrossRefGoogle Scholar
- 94.Midgley SE, Christiansen CB, Poulsen MW, Hansen CH, Fischer TK. Emergence of enterovirus D68 in Denmark, June 2014 to February 2015. Euro Surveill. 2015;20(17).Google Scholar
- 95.Roda D, Perez-Martinez E, Cabrerizo M, Trallero G, Martinez-Planas A, Luaces C, et al. Clinical characteristics and molecular epidemiology of Enterovirus infection in infants <3 months in a referral paediatric hospital of Barcelona. Eur J Pediatr. 2015;174:1549–53.PubMedCrossRefGoogle Scholar
- 96.Bal A, Schuffenecker I, Casalegno JS, Josset L, Valette M, Armand N, et al. Enterovirus D68 nosocomial outbreak in elderly people, France, 2014. Clin Microbiol Infect. 2015;21:e61–2.PubMedCrossRefGoogle Scholar
- 97.Parody R, Rabella N, Martino R, Otegui M, del Cuerpo M, Coll P, et al. Upper and lower respiratory tract infections by human enterovirus and rhinovirus in adult patients with hematological malignancies. Am J Hematol. 2007;82(9):807–11.PubMedCrossRefGoogle Scholar
- 98.Greninger AL, Naccache SN, Messacar K, Clayton A, Yu G, Somasekar S, et al. A novel outbreak enterovirus D68 strain associated with acute flaccid myelitis cases in the USA (2012–14): a retrospective cohort study. Lancet Infect Dis. 2015;15(6):671–82.PubMedCrossRefGoogle Scholar
- 99.Messacar K, Schreiner TL, Maloney JA, Wallace A, Ludke J, Oberste MS, et al. A cluster of acute flaccid paralysis and cranial nerve dysfunction temporally associated with an outbreak of enterovirus D68 in children in Colorado, USA. Lancet. 2015;385(9978):1662–71.PubMedCrossRefGoogle Scholar
- 100.Waghmare A, Pergam SA, Jerome KR, Englund JA, Boeckh M, Kuypers J. Clinical disease due to enterovirus D68 in adult hematologic malignancy patients and hematopoietic cell transplant recipients. Blood. 2015;125(11):1724–9.PubMedPubMedCentralCrossRefGoogle Scholar
- 101.Centers for Disease Control. Enterovirus D68 (EV-D68) 2014 outbreak strain-specific real-time reverse transcription/polymerase chain reaction (rRT-PCR) assay instructions, Atlanta, GA, 2014. p. 1–13.Google Scholar
- 102.Abzug MJ, Keyserling HL, Lee ML, Levin MJ, Rotbart HA. Neonatal enterovirus infection: virology, serology, and effects of intravenous immune globulin. Clin Infect Dis. 1995;20(5):1201–6.PubMedCrossRefGoogle Scholar
- 103.Yen MH, Huang YC, Chen MC, Liu CC, Chiu NC, Lien R, et al. Effect of intravenous immunoglobulin for neonates with severe enteroviral infections with emphasis on the timing of administration. J Clin Virol. 2015;64:92–6.PubMedCrossRefGoogle Scholar
- 104.Desmond RA, Accortt NA, Talley L, Villano SA, Soong SJ, Whitley RJ. Enteroviral meningitis: natural history and outcome of pleconaril therapy. Antimicrob Agents Chemother. 2006;50(7):2409–14.PubMedPubMedCentralCrossRefGoogle Scholar
- 105.Hayden FG, Coats T, Kim K, Hassman HA, Blatter MM, Zhang B, et al. Oral pleconaril treatment of picornavirus-associated viral respiratory illness in adults: efficacy and tolerability in phase II clinical trials. Antivir Ther. 2002;7(1):53–65.PubMedGoogle Scholar
- 106.Hayden FG, Herrington DT, Coats TL, Kim K, Cooper EC, Villano SA, et al. Efficacy and safety of oral pleconaril for treatment of colds due to picornaviruses in adults: results of 2 double-blind, randomized, placebo-controlled trials. Clin Infect Dis. 2003;36(12):1523–32.PubMedCrossRefGoogle Scholar
- 107.Pevear DC, Hayden FG, Demenczuk TM, Barone LR, McKinlay MA, Collett MS. Relationship of pleconaril susceptibility and clinical outcomes in treatment of common colds caused by rhinoviruses. Antimicrob Agents Chemother. 2005;49(11):4492–9.PubMedPubMedCentralCrossRefGoogle Scholar
- 108.Abzug MJ, Michaels MG, Wald E, Jacobs RF, Romero JR, Sanchez PJ, et al. A randomized, double-blind, placebo-controlled trial of pleconaril for the treatment of neonates with enterovirus sepsis. J Pediatric Infect Dis Soc. 2016;5(1):53–62.PubMedCrossRefGoogle Scholar
- 109.van der Linden L, Wolthers KC, van Kuppeveld FJ. Replication and inhibitors of enteroviruses and parechoviruses. Viruses. 2015;7(8):4529–62.PubMedPubMedCentralCrossRefGoogle Scholar
- 110.Allander T, Tammi MT, Eriksson M, Bjerkner A, Tiveljung-Lindell A, Andersson B. From the cover: Cloning of a human parvovirus by molecular screening of respiratory tract samples. Proc Natl Acad Sci U S A. 2005;102(36):12891–6.PubMedPubMedCentralCrossRefGoogle Scholar
- 111.Bastien N, Brandt K, Dust K, Ward D, Li Y. Human bocavirus infection, Canada. Emerg Infect Dis. 2006;12(5):848–50.PubMedPubMedCentralCrossRefGoogle Scholar
- 112.Martin ET, Fairchok MP, Kuypers J, Magaret A, Zerr DM, Wald A, et al. Frequent and prolonged shedding of bocavirus in young children attending daycare. J Infect Dis. 2010;201(11):1625–32.PubMedPubMedCentralCrossRefGoogle Scholar
- 113.Martin ET, Kuypers J, McRoberts JP, Englund JA, Zerr DM. Human bocavirus 1 primary infection and shedding in infants. J Infect Dis. 2015;212:516–24.PubMedPubMedCentralCrossRefGoogle Scholar
- 114.Schenk T, Strahm B, Kontny U, Hufnagel M, Neumann-Haefelin D, Falcone V. Disseminated bocavirus infection after stem cell transplant. Emerg Infect Dis. 2007;13(9):1425–7.PubMedPubMedCentralCrossRefGoogle Scholar
- 115.Schenk T, Maier B, Hufnagel M, Strahm B, Kontny U, Neumann-Haefelin D, et al. Persistence of human bocavirus DNA in immunocompromised children. Pediatr Infect Dis J. 2011;30(1):82–4.PubMedCrossRefGoogle Scholar
- 116.Waggoner J, Deresinski S. Rare and emerging viral infection in the transplant population. In: Safdar A, editor. Principles and practice of transplant infectious diseases. Berlin: Springer Medizin; 2013.Google Scholar
- 117.Schildgen O, Muller A, Allander T, Mackay IM, Volz S, Kupfer B, et al. Human bocavirus: passenger or pathogen in acute respiratory tract infections? Clin Microbiol Rev. 2008;21(2):291–304. table of contents.PubMedPubMedCentralCrossRefGoogle Scholar
- 118.Miyakis S, van Hal SJ, Barratt J, Stark D, Marriott D, Harkness J. Absence of human Bocavirus in bronchoalveolar lavage fluid of lung transplant patients. J Clin Virol. 2009;44(2):179–80.PubMedCrossRefGoogle Scholar
Copyright information
Open Access This chapter is distributed under the terms of the Creative Commons Attribution Noncommercial License, which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.


text: Frenemies: Millennium & NY DEC Fight Riverkeeper on Pipeline Upgrade December 6, 2017 Anti-Drilling, Energy Services, Industrywide Issues, Litigation, Millennium Pipeline, New York, Orange County, Pipelines, Regulation, Statewide NY Username Password Remember me Forgot Password? Join Us Related Post navigation UGI Pipeline to Feed Scranton NatGas-Fired Power Plant "On Track"Eagle's Nest Latest Wrinkle in Building 7.8 Mile Pipe to NY Power Plant You do not have permission to view the comments. Click here to cancel reply.Please Login to post a comment Notify me of follow-up comments by email.


text:
Find the Perfect Bra—No Fitting Required GET STARTED
Munki Munki
Munki Munki Fancy Coffee Classic Flannel PJs MO1692
FREE SHIPPING IN THE U.S. On Orders Over $80! It's simple. U.S. orders only. Learn more.
Need Help? Contact us! Monday-Friday 9am -7pm (EST)
One of winter's best friends, these classic flannel pajamas from Munki Munki, crafted with snuggle-worthy flannel, fit and feel comfortable--not just for sleep--they're perfect for curling up with a good book on a chilly evening.
- 2-Piece set
- Long sleeve, button front top
- Long pant bottoms
- Contrasting trim, cuffs and hem
- Full elastic waistband with drawstring
- Fancy coffee cups print
- Side pockets on pants, patch pocket on top
- Snap hems for adjustable length
Fit Info
- Fits True to Size
- Top: Bamboo rayon/cotton/spandex, Bottom: Bamboo rayon/cotton
- Imported
- Machine wash cold, tumble dry


text:
ConnectAd is excited to have been accepted as a Google AdWords Certified Partner. The designation is only given to companies with proven expertise and experience in managing Google AdWord campaigns, requiring partners to pass knowledge exams and actively manage more than $10,000 in the past 90 days.
For any charities who may be interested in outsourcing their Google Grants campaigns to experienced managers, you can be confident in our level of service and knowledge to you. To read more about how we're helping charities, please visit our testimonials page.


text:
Increasing organizational efficiency with leadership development.
Latest research indicates that 11-29% of team performance is determined by the operation of leadership. Developing competencies and leadership operation is one of the most effective means of increasing organizational performance.
Why introduce dynamic performance management?
Performance management systems can greatly contribute to establishing and sustaining organizational efficiency, however, only if it is run correctly. Incorrect performance management costs much and brings little.
How can we create cooperative organizational cultures?
Transforming culture is particularly difficult because permanent change can only be achieved by shaping the deeper layers of organisations, through a personal, inner transformation of individuals.


text:
India's first railway varsity to function from picturesque Pratap Vilas palace in Vadodara
The university will be offering two courses -- Bachelor of Science in Transportation Technology and a Bachelor of Business Administration in Transport Management.
Published: 05th September 2018 11:37 AM | Last Updated: 05th September 2018 11:37 AM | A+A A-
PM Narendra Modi, on Wednesday, September 5, will inaugurate India's first-ever Railway University at Vadodara in Gujarat. This university will function from the picturesque Pratap Vilas Palace, which currently houses the National Academy of Indian Railways - the alma mater for the Officers of the Indian Railways.
The university will be offering two courses -- Bachelor of Science in Transportation Technology and a Bachelor of Business Administration in Transport Management.
According to an Indian Express report, the university will function temporarily from the premises of the Pratap Vilas palace as the railway ministry has already identified a 100-acre plot in Vadodara to set up a greenfield campus.
The majestic Pratap Vilas palace was designed based on a renaissance design by British architect Charles F Stevens, son of F.W. Stevens who designed the famous Victoria Terminus of Bombay. The palace was constructed between 1908-1914 at the centre of 55 acres land, with a huge garden surrounded by several varieties of trees.
It was named after the 13th Maharaja of Baroda state, Pratapsinh Rao Gaekwad. The premises were taken over on lease in 1949 by the Bombay province who gave it to Indian Railways for use.
The National academy of Indian Railways, which was founded in 1930 at Premnagar, Dehradun was later shifted to Pratap Vilas palace in 1952. The palace now houses the Railway Staff College. This is the main training ground of Indian Railways.


text:
Is it OK to only have one sugar glider?
A: A single sugar glider in a cage is a miserable creature, and he may get so depressed he dies. While you are able to buy a single sugar glider from us, we do highly recommend that you buy two or more if you don't already have one at home. Sugar gliders are very social animals, and truly thrive when they have another glider with them. Sugar gliders will not die from ACTUAL loneliness. A lonely sugar glider deprived of social interaction WILL NOT thrive. They will become depressed and lonely, which can cause them to die. Lonely sugar gliders will become untamable and start to self mutate themselves. A lonely sugar glider may not bond with you until he has a mate. Sugar gliders will chew off their own tails, which will not grow back. They will start to chew off their own fingers, then they will eventually die. It's really no joke, they need the companion of a mate. They sleep in a tight ball hugging each other. I personally like to call them spooners.
Having just one sugar glider is like putting a 4 year old child in solitary confinement. Will the child survive? Yes, but the child won't be very sane after a short time. It's just cruel to the glider. I have been told by uneducated glider owners, that they spend all their time with their glider, so they aren't lonely. Not true, you can not replace another sugar glider.
One of the best toys for a sugar glider is another sugar glider. Two or more gliders will race around their cage in games of tag, hide-and-seek, and follow the leader. They will spend a lot of time in joint play and then snuggle together in their nest for a nap. They will groom each other, "talk" to each other, and keep each other occupied whenever you aren't available to interact with them. Their need for company is as comprehensive as their need for food.


text: Mature mom xxx nylons achives clips Recommend For You From: Meztira Category: Romanian Added: 28.06.2019 Share this video: Paula. Age:22. Slender, beautiful, affectionate, loving, Busty, athletic figure, elastic ass. Matures & Pantyhose Matures & Pantyhose Archives – Mature tube videos Milady Goddess of Gratification. Age:26. I am in search of a caring friend and a desired lover. I really want to feel welcome. 15 matures and pantyhose 16 legs On The Agenda Hottest Tags Naked girls on penisUsc song girl nudeNude couple with penisKatie kush pov Hot porn free compilationsCreampie step mom asianEbony black sexy girls videosBusty girl fat manBabe bang bukkake gangOld redhead mom nude Most Viewed: Hard strapon fuck free clips Michelle pfeiffer hot xxx Ed edd n eddy xxx Granny fuck xxx Amateur my friends hot mom Mature hairy moms pics Video clips teen sex Ebony mom and daughter fuck daddy Free xxx black teen movie Mature couple seduce young xxx Add a comment Enter the code from the image:Send Kajizragore 2 years ago Linda, maravilhosa. Ser elogiada Г© pouco pra vc. Douzil 2 years ago It does not make you shit that you deem that you are. It is not my job to provide you with a story that you will deny. Nikolkis 2 years ago Sorry for using the bad language in my earlier post Faukora 2 years ago What's the name of the song at the beginning? Zurisar 2 years ago WEB CAM .YEP YOU SHOULD. WHY NOT?


text:
US Senator Bernie Sanders, one of the candidates in the Democratic party's presidential primaries, on Wednesday once again suggested that the United States should rethink its policies toward Israel and the Palestinian Arabs.
Speaking during a televised debate of Democratic presidential candidates, Sanders said, "It is no longer good enough for us to be simply pro-Israel. I am pro-Israel. But we must treat the Palestinian people as well with the respect and dignity they deserve."
He also called the situation in Gaza "unsustainable," citing the high levels of unemployment there.
Sanders has come under fire for his statements against Israel, most recently when he told the J Street conference that the US should redirect its aid to Israel and give it to Gaza instead, while calling the Israeli government "racist".
Israel's Ambassador to the United Nations, Danny Danon, criticized Sanders' comments on Sunday, saying, "Perhaps Mr. Sanders didn't hear about Israel leaving Gaza in 2005. Maybe he hasn't had the chance to visit the Kerem Shalom crossing, where hundreds of trucks pass daily to provide humanitarian aid to Gaza. Maybe he doesn't know about the terror tunnels."
Danon added the Vermont Senator "is suggesting to give less military assistance to the United States' most important ally in the Middle East in order to give it to Hamas, a terrorist organization that celebrated the tragedy of 9/11."
Sanders' comments were also criticized by Nikki Haley, the former US Ambassador to the UN.
"Just when you thought Bernie Sanders couldn't get any more radical, he outdid himself. He wants to take money we give to Israel to defend itself from terrorists, and give it to Gaza, which is run by terrorists?? Unreal. Why isn't every other Dem pres candidate saying he's wrong?" tweeted Haley.
In August, Sanders said the US cannot prioritize the wants and needs of Israel over all else if it wants to help bring peace to the Middle East.
Last year, he criticized Netanyahu and his policies, saying, "As someone who believes absolutely and unequivocally in Israel's right to exist... we must say loudly and clearly, that to oppose the reactionary policies of Prime Minister Netanyahu does not make us anti-Israel."


text:
Suede and leather craft limited 60s black rabbit fur long belted trench.
32" waist
17" shoulder to shoulder
36" long
If you live in Austin and want to pick up in store, just use coupon code PICKMEUP at checkout to waive the shipping fee! For international shipping rates, please send inquiries to our CONTACT page.


text:
forced fucked african slaves » Music » Galeries de satin amateur gratuites
Galeries de satin amateur gratuites
- Category: Music
- Tags: galeries+de+satin+amateur+gratuites
Free female pants peeing photos video Where can i take the test at the 05 sec speed? So a furry got offended and banned Quackity Omg I can't believe they're learning this this is literally how everyone eats in europe : Fucking old sexy woman. And they'll all be surprised when the next ones swimming with this eating machine get bit in half of just swallowed whole oh why would it do that. I like the Minecraft music in the background Man sex albany. If im u i will call beacause ur mom slap u Miss teen usa Lebisan licking shaved pussy Ok I not into this story it needs to be scarier.
Danielle Panabaker. Age: 23. Gorgeous girl brighten up your loneliness for today! My body will not leave anyone indifferent. Silk skin, sweet face, elastic chest and ass.
Galeries De Satin Amateur Gratuites vintage men speedo galleries
Young Free Porn Galleries galeries de satin amateur gratuites
Excellent fan movie, Can't wait for episode 2 I think makeup forever and fenty was The best one Who looked Good on you: Jeremy lin got a ring before chris paul Okay, the Halloween vid with all three collaborators asking which palette you were using? Hon, I'm super proud but your foreshadowing in your editing makes me even prouder Of course kim soekjin is number one for me. Giada delaurentis nude picyures That first guy is a prick and a complete Asshole pardon my language but he's a dick The salt and ice to make ice cream worked because the salt and ice combined lowered the freezing temperature I just know it cuz I did this lab last year for chem Outcomes of masturbation. We need like ariana grande with a "new boyfriend". The dislikes could of came from the fact that some didn't like the ending to the video It's a theory, May or may not be true, you never know Great video, but seeing the expensive HUDA palettes being destroyed made me want to cry I want them all. You sound dumb with your messy ass! My twin brother was born 5 second early than me my mom said my brother was almost died thank God he's fine now.
Chelsea. Age: 24. Passionate and very sexy girl is waiting for you for the realization of your most cherished intimate desires. Sincere warmth and tenderness, and an unforgettable orgasm!
Contributions exhibitions photos amateurs
Disney please take notes! This is how Star Wars is meant to be! This guy is a neoliberal, so don't trust him You should do a full face only using foundations In my opinion, it would be between the Morphe foundation and Fenty Beauty foundation.
Petite blonde gal riding a dick blonde lingerie office blonde lingerie office. Tired babe stripteases after job babe office babe office. Wonderful office lady in black outfit ebony legs lingerie ebony legs lingerie. Old cunt shows her black pantyhose ebony office pantyhose ebony office pantyhose.
Porno retro gratuit
Galerie photo sur masturbation
Satin panty panties gallery pic orgasm
Amateur de galeria gratis video
Gay lesbian life looking
Dad fucked her again
Guy submissive cum sucking slut
Sexy barmaid wench pics
1 year ago
The fact that you are wearing some casual clothes really turns me on o.
1 year ago
good fucker....
1 year ago
I need to cancel the wall!
1 year ago
First off, my dick, then robots, fuck.


text:
A little too late – that was the downfall of the Montgomery Central Timberwolves' men's basketball team when they hosted the Anson Bearcats Jan. 28 at The Nest. The Timberwolves entered the fourth quarter down by almost 20 points. Senior Keyshon Ingram took over the game for the Timberwolves, scoring 12 of his game-high 33 points in a short burst in the fourth quarter, cutting the Bearcat lead to four points. The Bearcats called a time out, took control of the game and finished with a run of their own as the visitors left with a 91 – 79 victory.
To read the entire article, subscribe to Montgomery Herald by calling 910-576-6051 or go to www.montgomeryherald.com.


text:
You are not logged in.
Pages: 1
Hello! Is it possible to combine automatically generated mails GLPI into a conversation view in mail client? At the moment, a new letter arrives in the mail for each action, not uniting into a talk. I tried changing the title of the notification, but this no produce'd results. Mail (gmail, outlook) do not understand email's from glpi like a converstation.
Thanks a lot if you have any thoughts on this.
glpi 9.4.3
Pages: 1


text:
WASHINGTON — In a striking reversal, a top diplomat revised his testimony in the House impeachment inquiry to acknowledge that US military aid to Ukraine was being withheld until the foreign ally promised to investigate corruption as President Trump wanted.
The three-page update from US Ambassador Gordon Sondland, tucked beneath hundreds of pages of sworn testimony released Tuesday, provides new insight into Trump's push for Ukraine to investigate Democrats and Joe Biden in what the Democrats call a quid pro quo at the center of the House inquiry.
Specifically, Sondland said he now recalls telling a top aide to Ukraine President Volodymyr Zelenskiy, on the sidelines of a Warsaw meeting with US Vice President Mike Pence, that military aid to the country ''would likely not occur'' until Ukraine had provided a public anti-corruption statement ''as we have been discussing for many weeks.''
Trump has denied any quid pro quo, but Democrats say that is the singular narrative developing from the president's July 25 call with Zelenskiy . In that call, Trump, asked for ''a favor,'' the spark for the impeachment inquiry.
Rep. Adam Schiff, D-Calif., the chairman of the Intelligence Committee, said the House panels conducting the inquiry are releasing the word-by-word transcripts of the past weeks' closed-door hearings so the American public can decide for themselves.
''This is about more than just one call,'' Schiff wrote Tuesday in an op-ed in USA Today. ''We now know that the call was just one piece of a larger operation to redirect our foreign policy to benefit Donald Trump's personal and political interests, not the national interest.''
Pushing back, Trump Press Secretary Stephanie Grisham issued a statement saying the transcripts ''show there is even less evidence for this illegitimate impeachment sham than previously thought.''
House investigators released transcripts from Sondland, a wealthy businessman who donated $1 million to Trump's inauguration and is the US ambassador to the European Union, and from Kurt Volker, the former special envoy to Ukraine. The panels also announced they want to hear from Trump's acting chief of staff, reaching to the highest levels of the White House.
The documents include dozens of pages of text messages as the diplomats tried to navigate the demands of Rudy Giuliani, the president's personal lawyer, who they soon learn is running a back channel US foreign policy on Ukraine.
Sondland testified that he spoke with Secretary of State Mike Pompeo about Giuliani, ''and Pompeo rolled his eyes and said: 'Yes, it's something we have to deal with.'''
Pressed by investigators, Sondland -- who initially said he didn't know that the Ukraine firm Burisma that Trump wanted to investigate was linked to the Biden's son, Hunter -- also testified that it would be improper for the US to prompt Ukraine to investigate the Biden family. ''It doesn't sound good.''
In his revised testimony, Sondland says his memory was refreshed by the opening statements of two other inquiry witnesses, the top US diplomat in Ukraine, William Taylor, and Tim Morrison, a European expert at the National Security Council.
Sondland also told investigators Trump was in a ''bad mood'' and nearly hung up on him when he asked specifically whether the White House was withholding military aid for the investigation.
''I want nothing. I want no quid pro quo,'' Trump said, according to Sondland. ''I want Zelenskiy to do the right thing.''
Public hearings could begin as soon as next week in the impeachment inquiry that Trump says is illegitimate and Republicans in Congress call a sham.
The release of more transcripts comes as the Trump administration resumes its stonewalling of the inquiry. Two more White House officials, an energy adviser and a budget official, declined to appear Tuesday before investigators, even after one received a subpoena .
Meanwhile, Investigators say they want to hear from chief of staff Mick Mulvaney because his news conference last month amounted to ''nothing less than a televised confession'' of Trump's efforts to have Ukraine investigate Democrats and Biden as the White House was blocking military funding for the Eastern European ally.
Trump says he did nothing wrong, and Mulvaney later walked back his remarks.
The White House has instructed its officials not to comply with the impeachment inquiry being led by House Democrats. It is uncertain if Mulvaney will appear.
Republicans have been unable to deliver a unified argument against the impeachment probe, but one of them, Senate Majority Leader Mitch McConnell, said Tuesday he's ''pretty sure'' how it all will end.
''I don't think there's any question it would not lead to a removal'' of Trump from the White House, McConnell said.
Most of those who have testified before the House panel are from the ranks of the State Department, including recalled US Ambassador to Ukraine Marie Yovanovitch , whose testimony was released Monday.
Volker and Sondland both testified they were disappointed after briefing Trump at the White House upon their return from Zelenskiy's inauguration in May as a new leader of the young democracy vowing to fight corruption.
That pivotal May 23 meeting raised red flags when Trump thought told them to work with Giuliani, his personal attorney, on Ukraine issues.
Trump ''went on and on and on about how Ukraine is a disaster and they're bad people,'' Sondland testified.
Trump holds an alternative view that it was Ukraine, not Russia, that interfered in the 2016, a theory counter to US intelligence. '''They tried to take me down.' He kept saying that over and over,'' Sondland said.
Associated Press writers Colleen Long, Matthew Lee, Matthew Daly, Alan Fram, Andrew Taylor and Padmananda Rama contributed to this report.


text:
what does this message mean
When I charge a model When I load a model, PSSE gives me this message
Messages for api ADDMODELLIBRARY LIBRARY NOT FOUND (004060)
First time here? We are a friendly community of Power Systems Engineers. Check out the FAQ!
When I charge a model When I load a model, PSSE gives me this message
Messages for api ADDMODELLIBRARY LIBRARY NOT FOUND (004060)
In my machine I have a versión 33.5 PSSE but The error is displayed when trying to load a dll. however my partner has the same version of PSSE 33.5 and he can load the dll without any problema
That's weird, have you tried copying the files from your partners computer? Can't think of much else other than the directory is not accessible somehow. But I see Jconto mentioned this to you already in another thread.
I believe this message is indicating that PSSE failed to load the dynamics data from the provided .dll file.
I am not going to pretend to be an expert. However I have had this issue myself, I believe it can be caused by a few things. The ones i know of are as follows.
Ensure the .dll file is for correct version of PSSE, i.e. a dll file compiled for V32 cannot be used in V33.
In my particular case the .dll file was simply not compiled properly.
Lastly i'm not sure if this will cause this error to occur but if you did not have the fortran compiler, it might cause this issue to occur, happy to be corrected on any of these though. Hope this helps.
Asked: 2018-06-28 16:53:03 -0500
Seen: 184 times
Last updated: Jul 05 '18