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Case presentation: An 86-year-old female presented to our emergency department with chest pain and orthopnea and was diagnosed with heart failure and ST-elevation myocardial infarction, prompting hospitalization. During hospitalization, she developed a fever. A chest and abdominal contrast-enhanced computed tomography (CT), conducted to investigate the cause of the fever, coincidentally revealed sedimentation of contrast agent in the descending aorta. To differentiate from aortic dissection, we conducted dynamic CT, and it was confirmed that the contrast agent within the aorta decreased over time. On the same day, an echocardiogram revealed a left ventricular ejection fraction of 36% with reduced contractile function, and a stagnant, hazy echo within the descending aorta.Discussion: In aortic dissection, the retention of contrast agent in the false lumen of the aorta is a crucial finding for diagnosis. However, we experienced a case where contrast agent accumulated in the descending aorta, caused by low ejection fraction of the left ventricle. Differential diagnosis from aortic dissection may be possible due to the gradual decrease in contrast agent over time. This case is valuable to report given the limited number of previous reports on this phenomenon.

A novel motion stimulus is perceived to last longer than the subsequent motion stimulus moving in the opposite direction. A previous study suggested that the discrepancy in the processing latency for different onset types, as measured by reaction time, may play a role in this duration expansion. The present study examined whether the speed of motion stimuli influences this duration expansion. Experiment 1 demonstrated that the duration expansion ceased to occur when the stimulus speed increased. Experiment 2 showed that the increase in the speed reduced the reaction time for various onset types. However, the size of the changes in the reaction time did not match the reduction in the magnitude of the duration expansion observed in Experiment 1. These results suggest that the increase in speed eliminates the duration expansion of the novel motion stimulus, but the difference in the processing latency alone may not be the sole mechanism. [ABSTRACT FROM AUTHOR]

The regulation of inflammatory responses and pulmonary disease during SARS-CoV-2 infection is incompletely understood. Here we examine the roles of the prototypic pro- and anti-inflammatory cytokines IFNγ and IL-10 using the rhesus macaque model of mild COVID-19. We find that IFNγ drives the development of 18fluorodeoxyglucose (FDG)-avid lesions in the lungs as measured by PET/CT imaging but is not required for suppression of viral replication. In contrast, IL-10 limits the duration of acute pulmonary lesions, serum markers of inflammation and the magnitude of virus-specific T cell expansion but does not impair viral clearance. We also show that IL-10 induces the subsequent differentiation of virus-specific effector T cells into CD69+CD103+ tissue resident memory cells (Trm) in the airways and maintains Trm cells in nasal mucosal surfaces, highlighting an unexpected role for IL-10 in promoting airway memory T cells during SARS-CoV-2 infection of macaques. Author summary: Here we examine the roles of the prototypic pro- and anti-inflammatory cytokines IFNγ and IL-10 during SARS-CoV-2 infection of rhesus macaques. Whole body 18FDG-PET-CT imaging showed that IFNγ promotes SARS-CoV-2 induced pulmonary disease and IL-10 dampens the size, activity, and duration of lung lesions induced after infection. We also find a major role for IL-10 in the regulation of SARS-CoV-2-specific T cell responses. Our data show that IL-10 limits the magnitude of the effector T cell clonal burst during the acute phase of infection. We also find that following clearance of the virus, IL-10 promotes the differentiation of lung effector T cells into CD69+CD103+ tissue resident memory cells. [ABSTRACT FROM AUTHOR]

Blockade of the co-inhibitory receptor PD-1 enhances antitumor responses by boosting the function of antigen-specific T cells. Although rare, PD-1 blockade in patients with cancer can lead to exacerbation of infection-associated pathology. Here, we detail the case of a 38-year-old man who was enrolled in a clinical trial for assessment of the safety and activity of anti–PD-1 therapy for Kaposi sarcoma in people with HIV well-controlled on antiretroviral therapy. Less than a week after receiving the first dose of anti–PD-1 antibody (pembrolizumab), he presented with severe abdominal pain associated with sudden exacerbations of preexisting cytomegalovirus (CMV) enteritis and nontuberculous mycobacterial mesenteric lymphadenitis. Plasma biomarkers of gastrointestinal tract damage were highly elevated compared with healthy controls, consistent with HIV-associated loss of gut epithelial barrier integrity. Moreover, CMV-specific CD8 T cells expressed high levels of PD-1, and 7 days following PD-1 blockade, there was an increase in the frequency of activated CD38+ Ki67+ CMV-specific CD8 T cells. This case highlights the potential for PD-1 blockade to drive rapid exacerbations of inflammatory symptoms when administered to individuals harboring multiple unresolved infections. [ABSTRACT FROM AUTHOR]

With respect to the fossil resources shortage, the development of bio-based wood adhesives is an important research topic in wood science. There has been research on using sucrose for bio-based adhesives. However, a high acid catalyst content and a high hot-pressing temperature are required when manufacturing particleboards. In this study, to explore the possibility of p-toluenesulfonic acid (PTSA) as a promising acid catalyst for sucrose-based adhesives, the curing behavior of sucrose with PTSA (Suc-PTSA) was clarified. The thermal analysis results showed that the thermal properties of sucrose decreased significantly with the addition of PTSA. Based on the results of the insoluble matter rate, the optimal mixture ratio and heating conditions were determined to be 95:5 and 180 °C for 10 min, respectively. According to the results of FT−IR, the heat-treated Suc-PTSA contained furan compounds. In the context of the dynamic viscoelasticity, the onset temperature at which the storage modulus (E′) begins to rise was significantly lower than those of the other sucrose-based adhesives. PTSA has the potential to cure sucrose more efficiently and at lower temperatures than previous sucrose-based adhesives, making it a promising acid catalyst for sucrose. [ABSTRACT FROM AUTHOR]

Tirabrutinib is a highly selective Bruton's tyrosine kinase (BTK) inhibitor used to treat hematological malignancies. We analyzed the anti-tumor mechanism of tirabrutinib using phosphoproteomic and transcriptomic methods. It is important to check the drug's selectivity against off-target proteins to understand the anti-tumor mechanism based on the on-target drug effect. Tirabrutinib's selectivity was evaluated by biochemical kinase profiling assays, peripheral blood mononuclear cell stimulation assays, and the BioMAP system. Next, in vitro and in vivo analyses of the anti-tumor mechanisms were conducted in activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL) cells followed by phosphoproteomic and transcriptomic analyses. In vitro kinase assays showed that, compared with ibrutinib, tirabrutinib and other second-generation BTK inhibitors demonstrated a highly selective kinase profile. Data from in vitro cellular systems showed that tirabrutinib selectively affected B-cells. Tirabrutinib inhibited the cell growth of both TMD8 and U-2932 cells in correlation with the inhibition of BTK autophosphorylation. Phosphoproteomic analysis revealed the downregulation of ERK and AKT pathways in TMD8. In the TMD8 subcutaneous xenograft model, tirabrutinib showed a dose-dependent anti-tumor effect. Transcriptomic analysis indicated that IRF4 gene expression signatures had decreased in the tirabrutinib groups. In conclusion, tirabrutinib exerted an anti-tumor effect by regulating multiple BTK downstream signaling proteins, such as NF-κB, AKT, and ERK, in ABC-DLBCL. [ABSTRACT FROM AUTHOR]

High repetition rate, high reliability and long lifetime are required for pulsed power generators for environmental applications. Also, it is necessary to optimize the pulsed power generator for each environmental application. Recent developments in pulsed power generators are described. In addition, recent research of gaseous phase pollution control using pulsed power, cleaning of lake and dam of algae bloom by discharges, and recycling of concrete by pulsed power is summarized. Index Terms--Environmental application, pulsed power, discharge plasma, magnetic pulse compressor, streamer discharge, NOx removal, algae treatment, concrete recycling.

A pulsed discharge produced underwater has been an attractive method to treat waste water. For the optimization and realization of the water treatment system utilizing underwater pulsed discharge, modeling analysis could be one of the essential works. However, there is still no simulation work about the underwater pulsed discharge due to the lack of knowledge about its characteristic parameters such as electron temperature, electron density, and so on. In this paper, the temperature and the electron density in a pulsed discharge plasma produced underwater are measured and presented. A magnetic pulse compressor (MPC) was developed and used to create the electrical discharge in water. The developed MPC is all-solid state and is, therefore, a maintenance-free generator. To define the temperature and the electron density in an underwater pulsed discharge plasma, two kinds of spectroscopic measurements, called the line-pair method and Stark broadening, were carried out. According to the experimental results, the temperature and the electron density in the pulsed discharge plasma between point-plane electrodes immersed in water are determined to be 15 000 K and [10.sup.18]/[cm.sup.3], respectively. Index Terms--Discharge plasma, electron density, electron temperature, pulsed power, streamer discharge, underwater discharge.

Recently, cyanobacteria blooms (or water blooms) occurred on the surface of water bodies frequently and extensively due to eutrophia of the water. That has posed more and more serious environmental problems worldwide. In this paper, the effects of pulsed streamerlike discharge on M. aeruginosa cells are reported, which are one genus of cyanobacteria and ease to form water blooms. A stainless needle with a diameter of 30 [micro]m was employed as a point discharge electrode, which is 15-cm apart from the cylinder cathode, and a 2-[micro]s 160-kV pulse was applied. A pulsed streamerlike discharge was obtained in the water filled with cyanobacteria cells (named as sample water in this paper). From the experimental result, it can be found that the discharge collapsed the intracellular-structure gas vesicles in the M. aeruginosa ceils, and the colonies of the cells sank to the bottom of the discharge chamber and rotten gradually. Index Terms--Cyanobacteria, M. aeruginosa, pulse-forming network, streamerlike discharge.

This study investigated the subcellular localization of key enzymes of the glyoxylate cycle, i.e. isocitrate lyase (ICL; EC 4.1.3.1 ) and malate synthase (EC 2.3.3.9), that function constitutively in coordination with oxalate biosynthesis of glucose-grown Fomitopsis palustris. The ICL purified previously from F. palustris is termed FPICL1. Subcellular fractionation analysis of the cell homogenate by the sucrose density-gradient method showed that both key enzymes were present in peroxisomes, whereas acetyl-CoA synthase (EC 6.2.1.1 ) and oxalate-producing oxaloacetate acetylhydrolase (EC 3.7.1.1 ) were cytosolic. The peroxisomal localization of FPICL1 was further confirmed by electron microscopic and immunocytochemical analysis with anti-FPICL1 antibody. In addition, the peroxisomal target signal, composed of SKL at the C terminus of the cDNA encoding FPICL1, was found, which also suggests that FPICL1 is peroxisomal. Accordingly, it is postulated that transportation of succinate from peroxisomes to mitochondria, and vice versa, for the transportation of isocitrate or citrate, occurs in glucose-grown F. palustris for the constitutive metabolic coordination of the TCA and glyoxylate cycles with oxalate biosynthesis.

Background: Immune checkpoint inhibitor (ICI)-related myositis with myocarditis is a rare but potentially fatal immune-related adverse event. However, its clinical features, response to immunosuppressive treatment, and prognosis remain poorly understood. Here, we describe the clinical course of patients with ICI-related myositis overlapping with myocarditis treated at our institution and a systematic review focusing on the response to immunosuppressive therapy. Methods: We identified patients who developed ICI-induced myositis with myocarditis and were treated at our hospital using a retrospective chart review of electronic medical records. For the systematic review, studies reporting ICI-induced myositis with myocarditis were identified using the Cochrane Library and PubMed databases. Results: Of the 625 patients treated with ICIs, four developed myositis with concurrent myocarditis. All the patients received immunosuppressive therapy. We assessed the activity of myocarditis and myositis based on temporal changes in troponin and creatine kinase (CK) levels. In all patients, peak troponin values appeared later than the peak CK values (median, 17 days). The median time from the start of ICI therapy to the peak of troponin and CK levels was 42.5 and 28 days, respectively. In all patients, CK levels decreased rapidly and steadily after the initiation of immunosuppressants. However, troponin levels were unstable and increased. In all patients, CK levels normalized within one month (range, 12–27 days), but troponin levels took several months to normalize (range, 84–161 days). Fourteen cases of ICI-related myositis with myocarditis were included in the systematic review. Of the 14 cases, 12 (86%) had their CK level decreased after the initial steroid treatment, but the troponin level increased and was higher than that before the start of treatment. In addition, the peak troponin values appeared later than the peak CK values (a median of 6.5 days). Eight (89%) of 9 long-term follow-up patients had troponin levels above the normal range even after CK normalization. Conclusion: In most cases of ICI-related myositis with myocarditis, troponin levels increased after the initial steroid treatment despite decreased CK levels, and exceeded pre-steroid levels. In addition, troponin remained elevated for several months after CK normalized. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily replicates in mucosal sites, and more information is needed about immune responses in infected tissues. Here, we used rhesus macaques to model protective primary immune responses in tissues during mild coronavirus disease 2019 (COVID-19). Viral RNA levels were highest on days 1 to 2 after infection and fell precipitously thereafter. 18F-fluorodeoxyglucose (18FDG)–avid lung abnormalities and interferon (IFN)–activated monocytes and macrophages in the bronchoalveolar lavage (BAL) were found on days 3 to 4 after infection. Virus-specific effector CD8+ and CD4+ T cells became detectable in the BAL and lung tissue on days 7 to 10 after viral RNA, radiologic evidence of lung inflammation, and IFN-activated myeloid cells had substantially declined. SARS-CoV-2–specific T cells were not detectable in the nasal turbinates, salivary glands, and tonsils on day 10 after infection. Thus, SARS-CoV-2 replication wanes in the lungs, as well as the nasal and oral mucosa, of rhesus macaques before antigen-specific effector T cells arrive at those sites, suggesting that innate immunity efficiently restricts viral replication during mild COVID-19. [ABSTRACT FROM AUTHOR]

In the postpartum period, cows experience the uterine bacterial infection and develop the endometritis. To eliminate bacteria and recover from endometritis, endometrial epithelial and stromal cells secrete the cytokine and chemokine, such as interleukin 6 (IL‐6), IL‐8, and monocyte chemotactic protein 1 (MCP1), to recruit immune cells. Moreover, the symptom of endometritis is prolonged in summer and we have recently indicated that hyperthermia suppresses and enhances the IL‐6 production in response to lipopolysaccharide (LPS) challenge in endometrial epithelial and stromal cells, respectively. However, the mechanisms for the opposite reaction of IL‐6 secretion in response to LPS challenge in both types of endometrial cells under hyperthermia conditions were still unclear. To reveal these mechanisms, both types of endometrial cells were cultured with LPS under the control (38.5°C) or hyperthermia (40.5°C) conditions and comprehensively analyzed differential gene expressions of them by RNA‐seq. In addition, based on these results, we examined the effect of endoplasmic reticulum (ER) stress on the IL‐6 production in both types of endometrial cells cultured with LPS under hyperthermia conditions. In comprehensive analysis, hyperthermia induced the ER stress in the endometrial stromal cells but not in the endometrial epithelial cells. Actually, we confirmed that hyperthermia increased the gene expression of BiP, ATF4, and sXBP1 and protein expression of BiP and phosphorylated inositol requiring 1, ER stress marker, in the endometrial stromal cells but not in the endometrial epithelial cells. Moreover, in the endometrial stromal cells exposed to LPS, activation and inhibition of ER stress enhanced the IL‐6 production under control conditions and suppressed it under hyperthermia conditions, respectively. In this study, we could uncover the one of causes for the disruption of IL‐6 production in response to LPS challenge in the endometrial cells under hyperthermia conditions. This finding might be a clue for the improvement of the symptom of endometritis in cows during summer. [ABSTRACT FROM AUTHOR]

PD-1 blockade carries perils: The potentiation of T cell–mediated antitumor responses achieved in multiple types of cancer via inhibition of the PD-1 checkpoint pathway has led to suggestions that anti–PD-1 therapy might also boost T cell immunity in chronic infections including tuberculosis. Kauffman et al. examined the effect of anti–PD-1 antibody treatment on the clinical course of Mycobacterium tuberculosis (Mtb) infection in rhesus macaques. CD8 T cell responses were boosted in monkeys receiving anti–PD-1 infusions, but the stronger CD8 T cell responses were coupled with increases in proinflammatory cytokines, impaired CD4 T cell function, and higher bacterial loads in lung granulomas. These findings in a nonhuman primate model signal that anti–PD-1–based therapy needs to be used cautiously in patients with cancer with a history of Mtb exposure. Boosting immune cell function by targeting the coinhibitory receptor PD-1 may have applications in the treatment of chronic infections. Here, we examine the role of PD-1 during Mycobacterium tuberculosis (Mtb) infection of rhesus macaques. Animals treated with anti–PD-1 monoclonal antibody developed worse disease and higher granuloma bacterial loads compared with isotype control–treated monkeys. PD-1 blockade increased the number and functionality of granuloma Mtb-specific CD8 T cells. In contrast, Mtb-specific CD4 T cells in anti–PD-1–treated macaques were not increased in number or function in granulomas, expressed increased levels of CTLA-4, and exhibited reduced intralesional trafficking in live imaging studies. In granulomas of anti–PD-1–treated animals, multiple proinflammatory cytokines were elevated, and more cytokines correlated with bacterial loads, leading to the identification of a role for caspase 1 in the exacerbation of tuberculosis after PD-1 blockade. Last, increased Mtb bacterial loads after PD-1 blockade were found to associate with the composition of the intestinal microbiota before infection in individual macaques. Therefore, PD-1–mediated coinhibition is required for control of Mtb infection in macaques, perhaps because of its role in dampening detrimental inflammation and allowing for normal CD4 T cell responses. [ABSTRACT FROM AUTHOR]

After parturition, cows frequently develop uterine bacterial infections, resulting in the onset of endometritis. To eliminate the bacteria, bovine endometrial cells secrete chemokines, such as IL‐6 and MCP1, which attract macrophages (MΦs) to the subepithelial stroma. These attracted MΦs are not only involved in bacterial elimination but also the orchestration of inflammation and tissue repair. These immune responses aid in the recovery from endometritis; however, the recovery from endometritis takes longer in summer than in any other season. Based on these findings, we hypothesized that heat stress (HS) affects the chemokine production in endometrial cells. To confirm this hypothesis, we compared IL‐6 and MCP1 production induced by lipopolysaccharide (LPS) in bovine endometrial epithelial and stromal cells under normal (38.5°C) and HS conditions (40.5°C). In the endometrial epithelial cells, IL‐6 production stimulated by LPS was significantly (p <.05) suppressed under HS conditions. MCP1 production in endometrial epithelial cells was not detected under both the control and HS conditions regardless of the presence of LPS. Moreover, LPS significantly (p <.05) stimulated IL‐6 and MCP1 production in endometrial stromal cells. Moreover, HS significantly (p <.05) enhanced their production compared to that under the control conditions. In addition, HS did not affect the migration ability of MΦs; however, the supernatant of the endometrial stromal cells cultured under the HS condition significantly (p <.05) attracted the MΦs when compared to the control condition. These results suggest that HS disrupts chemokine production in two types of endometrial cells and alters the distribution of MΦs in the endometrium during the summer. [ABSTRACT FROM AUTHOR]

ZFP36L1 is an RNA-binding protein responsible for mRNA decay in the cytoplasm. ZFP36L1 has also been suggested as a nuclear-cytoplasmic shuttling protein because it contains a potential nuclear localization signal and a nuclear export signal. However, it remains unclear how the nuclear localization of ZFP36L1 is controlled. In this study, we provide evidence that the nuclear accumulation of ZFP36L1 protein is modulated in a cell cycle-dependent manner. ZFP36L1 protein accumulation in fractionated nuclei was particularly prominent in cells arrested at G1-/S-phase boundary, while it was downregulated in S-phase cells, and eventually disappeared in G2-phase nuclei. Moreover, forced nuclear targeting of ZFP36L1 revealed marked downregulation of this protein in S- and G2-phase cells, suggesting that ZFP36L1 can be eliminated in the nucleus. The C-terminal serine-rich cluster of ZFP36L1 is critical for the regulation of its nuclear accumulation because truncation of this probable disordered region enhanced the nuclear localization of ZFP36L1, increased its stability and abolished its cell cycle-dependent fluctuations. These findings provide the first hints to the question of how ZFP36L1 nuclear accumulation is controlled during the course of the cell cycle. [ABSTRACT FROM AUTHOR]

We give a characterization of alternating link exteriors in terms of cubed complexes. To this end, we introduce the concept of a “signed BW cubed-complex”, and give a characterization for a signed BW cubed-complex to have the underlying space which is homeomorphic to an alternating link exterior. [ABSTRACT FROM AUTHOR]

Recent data indicate that the differentiation state of Th1 cells determines their protective capacity against tuberculosis. Therefore, we examined the role of Th1-polarizing factors in the generation of protective and non-protective subsets of Mtb-specific Th1 cells. We find that IL-12/23p40 promotes Th1 cell expansion and maturation beyond the CD73+CXCR3+T-betdim stage, and T-bet prevents deviation of Th1 cells into Th17 cells. Nevertheless, IL- 12/23p40 and T-bet are also essential for the production of a prominent subset of intravascular CX3CR1+KLRG1+ Th1 cells that persists poorly and can neither migrate into the lung parenchyma nor control Mtb growth. Furthermore, T-bet suppresses development of CD69+CD103+ tissue resident phenotype effectors in lung. In contrast, Th1-cell-derived IFN-γ inhibits the accumulation of intravascular CX3CR1+KLRG1+ Th1 cells. Thus, although IL-12 and T-bet are essential host survival factors, they simultaneously oppose lung CD4 T cell responses at several levels, demonstrating the dual nature of Th1 polarization in tuberculosis. [ABSTRACT FROM AUTHOR]

IFN-γ–producing CD4 T cells are required for protection against Mycobacterium tuberculosis (Mtb) infection, but the extent to which IFN-γ contributes to overall CD4 T cell-mediated protection remains unclear. Furthermore, it is not known if increasing IFN-γ production by CD4 T cells is desirable in Mtb infection. Here we show that IFN-γ accounts for only ~30% of CD4 T cell-dependent cumulative bacterial control in the lungs over the first six weeks of infection, but >80% of control in the spleen. Moreover, increasing the IFN-γ–producing capacity of CD4 T cells by ~2 fold exacerbates lung infection and leads to the early death of the host, despite enhancing control in the spleen. In addition, we show that the inhibitory receptor PD-1 facilitates host resistance to Mtb by preventing the detrimental over-production of IFN-γ by CD4 T cells. Specifically, PD-1 suppressed the parenchymal accumulation of and pathogenic IFN-γ production by the CXCR3+KLRG1-CX3CR1- subset of lung-homing CD4 T cells that otherwise mediates control of Mtb infection. Therefore, the primary role for T cell-derived IFN-γ in Mtb infection is at extra-pulmonary sites, and the host-protective subset of CD4 T cells requires negative regulation of IFN-γ production by PD-1 to prevent lethal immune-mediated pathology. [ABSTRACT FROM AUTHOR]

Radiotherapy (RT) combined with immunotherapy is promising; however, the immune response signature in the clinical setting after RT remains unclear. Here, by integrative spatial and single-cell analyses using multiplex immunostaining (CODEX), spatial transcriptome (VISIUM), and single-cell RNA sequencing, we substantiated the infiltration of immune cells into tumors with dynamic changes in immunostimulatory and immunosuppressive gene expression after RT. In addition, our comprehensive analysis uncovered time- and cell type-dependent alterations in the gene expression profile after RT. Furthermore, myeloid cells showed prominent up-regulation of immune response-associated genes after RT. Notably, a subset of infiltrating tumor-associated myeloid cells showing PD-L1 positivity exhibited significant up-regulation of immunostimulatory (HMGB1 and ISG15), immunosuppressive (SIRPA and IDO1), and protumor genes (CXCL8, CCL3, IL-6, and IL-1AB), which can be targets of immunotherapy in combination with PD-L1. These datasets will provide information on the RT-induced gene signature to seek an appropriate target for personalized immunotherapy combined with RT and guide the timing of combination therapy. [ABSTRACT FROM AUTHOR]

Listeria monocytogenes induces the formation of inflammasomes and subsequent caspase-1 activation, and the adaptor apoptosis-associated speck-like protein containing a CARD (ASC) is crucial for this response. However, the role of ASC in L. monocytogenes infection in vivo is unclear. In this study, we demonstrate that ASC has a detrimental effect on host defense against L. monocytogenes infection at a lethal dose (106 CFU), but not at a sublethal dose (103 CFU). During lethal L. monocytogenes infection, serum levels of IL-18 and IL-10 were markedly elevated in WT mice, but not in ASC KO mice. IL-18 KO mice were more resistant to lethal L. monocytogenes infection than WT mice and had lower levels of serum IL-10. Furthermore, blockade of IL-10 receptor resulted in a reduction in bacterial counts, suggesting that ASC and IL-18might exacerbate L. monocytogenes infection through induction of IL-10. We noticed that maturation of IL-18 during lethal infection was partially independent of caspase-1, but was critically dependent on ASC. ASC was required for the elevation of serum neutrophil serine protease activity, which correlated with caspase-1-independent IL-18 maturation and IL-10 production. Collectively, these results suggest that ASC plays a detrimental role in lethal L. monocytogenes infection through IL-18 production in an inflammasome-dependent and -independent manner. [ABSTRACT FROM AUTHOR]

Th1 cells are critical for containment of Mycobacterium tuberculosis infection, but little else is known about the properties of protective CD4 T cell responses. In this study, we show that the pulmonary Th1 response against M. tuberculosis is composed of two populations that are either CXCR3hi and localize to lung parenchyma or are CX3CR1hiKLRG1hi and are retained within lung blood vasculature. M. tuberculosis-specific parenchymal CD4 T cells migrate rapidly back into the lung parenchyma upon adoptive transfer, whereas the intravascular effectors produce the highest levels of IFN-γ in vivo. Importantly, parenchymal T cells displayed greater control of infection compared with the intravascular counterparts upon transfer into susceptible T cell-deficient hosts. Thus, we identified a subset of naturally generated M. tuberculosis-specific CD4 T cells with enhanced protective capacity and showed that control of M. tuberculosis correlates with the ability of CD4 T cells to efficiently enter the lung parenchyma rather than produce high levels of IFN-γ. [ABSTRACT FROM AUTHOR]

Proteinis a soft material with inherently large structural disorder.Consequently, the bulk spectroscopies of photosynthetic pigment proteincomplexes provide averaged information where many details are lost.Here we report spectroscopy of single light-harvesting complexes wherefluorescence excitation and detection polarizations are both independentlyrotated. Two samples of peripheral antenna (LH2) complexes from Rhodopseudomonas acidophilawere studied. In one, the complexeswere embedded in polyvinyl alcohol (PVA) film; in the other, theywere anchored on the glass surface and covered by the PVA film. LH2contains two rings of pigment moleculesB800 and B850. TheB800 excitation polarization properties of the two samples were foundto be very similar, indicating that orientation statistics of LH2sare the same in these two very different preparations. At the sametime, we found a significant difference in B850 emission polarizationstatistics. We conclude that the B850 band of the anchored sampleis substantially more disordered. We argue that both B800 excitationand B850 emission polarization properties can be explained by thetilt of the anchored LH2s due to the spin-casting of the PVA filmon top of the complexes and related shear forces. Due to the tilt,the orientation statistics of two samples become similar. Anchoringis expected to orient the LH2s so that B850 is closer to the substrate.Consequently, the tilt-related strain leads to larger deformationand disorder in B850 than in B800. [ABSTRACT FROM AUTHOR]

In a photosynthetic membrane, nano-scale patterns of light-harvesting (LH) pigment-protein complexes play an essential role in capturing photons and ensuring efficient excitation energy transfer. LH complexes 1 and 2 have drawn attention as building blocks of a nano-scale photoelectric device. For obtaining a device with efficiency comparable to that of the natural photosynthesis, a method has to be established for forming a two-dimensional assembly of LH complexes around a metal electrode. In this study, LH2 complexes isolated from Rb. sphaeroides were immobilized on a patterned gold surface. Quenching of photo-excitation energy by gold was prevented through the placement of a self-assembled phospholipid monolayer between the LH2 complexes and the gold surface. [ABSTRACT FROM AUTHOR]

The article studies the effect of excess intake of leucine from dietary protein on serine dehydratase (SDH) in rat liver. The SDH activity in the liver of rats was strongly induced by excess leucine intake. It was accompanied by increases in the levels of SDH messenger RNA. The study also showed that isoleucine and valine had small effect on SDH induction.