Streptococcus Intermedius Brain and Diverticular Abscesses After Dental Manipulation: A Case Report.

A brain abscess is defined as a focal intracerebral infection consisting of an encapsulated collection of pus, which can be a life-threatening complication of infections, trauma, or surgery. While immunocompromised patients can have a wide array of causative organisms, bacterial species represent the most common etiology in immunocompetent individuals. The incidence of brain abscesses ranges from 0.4 to 0.9 per 100,000, with a high predisposition among immunocompromised patients and in those with disruption of the blood-brain barrier. The most common causative organisms found were Streptococcus species, particularly S. viridians and S. pneumonia, Enterococcus, and Staphylococcus species, mainly S. aurieus and S. epidermidis. Microorganism can invade the brain through different mechanisms, either directly by contiguous spread and odontogenic infections, which usually cause a single brain abscess, or indirectly through hematogenous spread which can cause multiple brain abscesses. Both surgical and conservative dental procedures contribute to hematogenous spreading of oral microorganisms. Although most of those organisms are eliminated shortly after they gain access to the bloodstream, some can persist and contribute to the pathogenesis of abscesses in the appropriate environment. Odontogenic origins are rarely implicated in the formation of brain abscesses, and oral foci comprise approximately 5% of identified cases. We report a case of brain and diverticular abscesses due to S. intermidius occurring two months after dental extraction. This case highlights the fact that even usual dental workup can result in the development of bacteremia and disseminated abscesses including but not restricted to the brain. Consequently, in addition to identifying the possible source of bacteremia with an extensive history and physical exam, the diagnosis of Streptococcus milleri organisms should prompt the physicians to screen for sites of possible metastatic infection spread

Acute Liver Failure in a COVID-19 Patient Without any Preexisting Liver Disease.

In December 2019, an outbreak of novel coronavirus started in Wuhan, China, which gradually spread to the entire world. The World Health Organization (WHO) on February 11, 2020, officially announced the name for the disease as coronavirus disease 2019, abbreviated as COVID-19. It is caused by severe respiratory distress syndrome coronavirus 2 (SARS-CoV-2). The WHO declared SARS-CoV-2 as a pandemic on March 11, 2020. SARS-CoV-2 mainly causes fever as well as respiratory symptoms such as cough and shortness of breath. Gastrointestinal/hepatic sequelae such as diarrhea, nausea, vomiting, and elevated liver enzymes have been reported as well. Studies and data so far on coronavirus infections from China, Singapore, and other countries showed that liver enzymes elevation could be seen in 20-50% of cases. More severe disease can correlate with the worsening of liver enzymes. However, acute liver failure in patients with COVID-19 has not been described. Herein we report a case of acute liver failure in an elderly patient with COVID-19 infection who did not have a history of preexisting liver disease

Hepatitis C Infection Patterns at a Tertiary Care Center in New York: A Cross-Sectional Study.

Introduction In the United States, 2.7 to 3.9 million patients are infected with the hepatitis C virus (HCV) with 3,500 new cases reported yearly. According to the Centers for Disease Control and Prevention, HCV was the underlying or contributing cause of death of 19,659 patients in 2014. These facts underscore the need for a better understanding of the scope of this disease. Our epidemiologic study aimed at analyzing the pattern of occurrence of HCV infection at Staten Island University Hospital (SIUH) by evaluating the characteristics of newly infected patients with hepatitis C in 2014. The identified features served to better distinguish the targets for preventive health care in our particular population. Methodology A cross-sectional study of all newly diagnosed patients with HCV infections in the year 2014 presenting to SIUH was conducted using International Classification of Disease-9 codes (ICD-9) for hepatitis C. We included all patients with a positive HCV antibody confirmed by polymerase chain reaction testing. Patients were divided into groups according to age to simulate the age groups in the 2013 - 2014 Hepatitis B and C Annual Report of the New York City (NYC) Department of Health and Mental Hygiene published in 2016 (abbreviated to 2014 NYCDOH Report, hereafter). Gender and HCV genotypes were also collected. We compared disease frequency between age groups, gender, and genotype with the results of the 2014 NYCDOH Report. Results A total of 378 newly diagnosed HCV cases were identified; 60.05% were men, and 39.95% were women. The rate of infection with genotype 1a was the highest (36. 5%) followed by 1b (25.9%). In women, genotype 1b was predominant (13.76%) versus genotype 1a as the most common in men. The mean age was 54 years for men and 57 years for women. Most cases fell into the 60 to 69-year age group (32.28%), followed by the 50 to 59-year age group (31.48%). More so, all patients 80 years and older were exclusively women. Conclusions We found most new HCV infections at SIUH were diagnosed in patients aged 60 to 69 years, and the 2014 NYC DOH Report indicates most new HCV infections occur in patients aged 40 to 59 years. Also, all HCV infections detected in patients older than 80 years of age were found in women. These findings provide a better understanding of the patient demographics for appropriate HCV screening policies. Increased awareness and strict adherence to screening policies in baby boomers and high-risk populations are paramount in order to diagnose HCV infection early, offer therapy, and prevent HCV-related mortality and morbidity

Recurrent mutualism breakdown events in a legume rhizobia metapopulation.

Bacterial mutualists generate major fitness benefits for eukaryotes, reshaping the host phenotype and its interactions with the environment. Yet, microbial mutualist populations are predicted to generate mutants that defect from providing costly services to hosts while maintaining the capacity to exploit host resources. Here, we examined the mutualist service of symbiotic nitrogen fixation in a metapopulation of root-nodulating Bradyrhizobium spp. that associate with the native legume Acmispon strigosus. We quantified mutualism traits of 85 Bradyrhizobium isolates gathered from a 700 km transect in California spanning 10 sampled A. strigosus populations. We clonally inoculated each Bradyrhizobium isolate onto A. strigosus hosts and quantified nodulation capacity and net effects of infection, including host growth and isotopic nitrogen concentration. Six Bradyrhizobium isolates from five populations were categorized as ineffective because they formed nodules but did not enhance host growth via nitrogen fixation. Six additional isolates from three populations failed to form root nodules. Phylogenetic reconstruction inferred two types of mutualism breakdown, including three to four independent losses of effectiveness and five losses of nodulation capacity on A. strigosus. The evolutionary and genomic drivers of these mutualism breakdown events remain poorly understood

Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis

Concurrent mutation of a RAS oncogene and the tumor suppressor p53 is common in tumorigenesis, and inflammation can promote RAS-driven tumorigenesis without the need to mutate p53. Here, we show, using a well-established mutant RAS and an inflammation-driven mouse skin tumor model, that loss of the p53 inhibitor iASPP facilitates tumorigenesis. Specifically, iASPP regulates expression of a subset of p63 and AP1 targets, including genes involved in skin differentiation and inflammation, suggesting that loss of iASPP in keratinocytes supports a tumor-promoting inflammatory microenvironment. Mechanistically, JNK-mediated phosphorylation regulates iASPP function and inhibits iASPP binding with AP1 components, such as JUND, via PXXP/SH3 domain-mediated interaction. Our results uncover a JNK-iASPP-AP1 regulatory axis that is crucial for tissue homeostasis. We show that iASPP is a tumor suppressor and an AP1 coregulator

Modelling of friction stir welding of DH36 steel

A 3-D computational fluid dynamics (CFD) model was developed to simulate the friction stir welding of 6-mm plates of DH36 steel in an Eulerian steady-state framework. The viscosity of steel plate was represented as a non- Newtonian fluid using a flow stress function. The PCBN-WRe hybrid tool was modelled in a fully sticking condition with the cooling system effectively represented as a negative heat flux. The model predicted the temperature distribution in the stirred zone (SZ) for six welding speeds including low, intermediate and high welding speeds. The results showed higher asymmetry in temperature for high welding speeds. Thermocouple data for the high welding speed sample showed good agreement with the CFD model result. The CFD model results were also validated and compared against previous work carried out on the same steel grade. The CFD model also predicted defects such as wormholes and voids which occurred mainly on the advancing side and are originated due to the local pressure distribution between the advancing and retreating sides. These defects were found to be mainly coming from the lack in material flow which resulted from a stagnant zone formation especially at high tra- verse speeds. Shear stress on the tool surface was found to in- crease with increasing tool traverse speed. To produce a “sound” weld, the model showed that the welding speed should remain between 100 and 350 mm/min. Moreover, to prevent local melt- ing, the maximum tool’s rotational speed should not exceed 550 RPM

Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis

Concurrent mutation of a RAS oncogene and the tumor suppressor p53 is common in tumorigenesis, and inflammation can promote RAS-driven tumorigenesis without the need to mutate p53. Here, we show, using a well-established mutant RAS and an inflammation-driven mouse skin tumor model, that loss of the p53 inhibitor iASPP facilitates tumorigenesis. Specifically, iASPP regulates expression of a subset of p63 and AP1 targets, including genes involved in skin differentiation and inflammation, suggesting that loss of iASPP in keratinocytes supports a tumor-promoting inflammatory microenvironment. Mechanistically, JNK-mediated phosphorylation regulates iASPP function and inhibits iASPP binding with AP1 components, such as JUND, via PXXP/SH3 domain-mediated interaction. Our results uncover a JNK-iASPP-AP1 regulatory axis that is crucial for tissue homeostasis. We show that iASPP is a tumor suppressor and an AP1 coregulator

Synaptic Depression Via Mglur1 Positive Allosteric Modulation Suppresses Cue-Induced Cocaine Craving

Cue-induced cocaine craving is a major cause of relapse in abstinent addicts. In rats, cue-induced craving progressively intensifies (incubates) during withdrawal from extended-access cocaine self-administration. After ~1 month of withdrawal, incubated craving is mediated by Ca(2+)-permeable AMPA receptors (CP-AMPARs) that accumulate in the nucleus accumbens (NAc). We found that decreased mGluR1 surface expression in the NAc preceded and enabled CP-AMPAR accumulation. Thus, restoring mGluR1 transmission by administering repeated injections of an mGluR1 positive allosteric modulator (PAM) prevented CP-AMPAR accumulation and incubation, whereas blocking mGluR1 transmission at even earlier withdrawal times accelerated CP-AMPAR accumulation. In studies conducted after prolonged withdrawal, when CP-AMPAR levels and cue-induced craving are high, we found that systemic administration of an mGluR1 PAM attenuated the expression of incubated craving by reducing CP-AMPAR transmission in the NAc to control levels. These results suggest a strategy in which recovering addicts could use a systemically active compound to protect against cue-induced relapse

MyD88 and STING Signaling Pathways Are Required for IRF3-Mediated IFN-β Induction in Response to Brucella abortus Infection

Type I interferons (IFNs) are cytokines that orchestrate diverse immune responses to viral and bacterial infections. Although typically considered to be most important molecules in response to viruses, type I IFNs are also induced by most, if not all, bacterial pathogens. In this study, we addressed the role of type I IFN signaling during Brucella abortus infection, a facultative intracellular bacterial pathogen that causes abortion in domestic animals and undulant fever in humans. Herein, we have shown that B. abortus induced IFN-β in macrophages and splenocytes. Further, IFN-β induction by Brucella was mediated by IRF3 signaling pathway and activates IFN-stimulated genes via STAT1 phosphorylation. In addition, IFN-β expression induced by Brucella is independent of TLRs and TRIF signaling but MyD88-dependent, a pathway not yet described for Gram-negative bacteria. Furthermore, we have identified Brucella DNA as the major bacterial component to induce IFN-β and our study revealed that this molecule operates through a mechanism dependent on RNA polymerase III to be sensed probably by an unknown receptor via the adaptor molecule STING. Finally, we have demonstrated that IFN-αβR KO mice are more resistant to infection suggesting that type I IFN signaling is detrimental to host control of Brucella. This resistance phenotype is accompanied by increased IFN-γ and NO production by IFN-αβR KO spleen cells and reduced apoptosis