Smart Ceiling Temperature Controlled Fan

Previous generation models requires more human efforts but in the age of modern era as every technology is being evolving into a more advanced an modified version by operating automatically so here in the same way this project work will reinvent the ceiling fan to make it smarter. Fans make people feel cooler but don’t lower a room’s actual temperature. So to save energy, it will run automatically according to the temperature of the surroundings and will get turn off below a particular temperature by itself. Considering already existing ceiling fans it is difficult to control the speed of each and every fan depending upon the weather conditions. The idea behind the paper smart ceiling temperature controlled fan is to control the speed of fan using microcontroller ATMEGA16, based on variations in temperature detected by temperature sensor. Besides house owners, this smart feature in a fan can also benefit schools, firms and other public buildings as they also have a certain regular routine. Therefore this project work is taken up to minimize human effort and save energy at the same time which is a need of an hour. The software used for this project is PROTEUS_V78i and WINAVR studio4

Quantum option pricing via the Karhunen-Lo\`{e}ve expansion

We consider the problem of pricing discretely monitored Asian options over $T$ monitoring points where the underlying asset is modeled by a geometric Brownian motion. We provide two quantum algorithms with complexity poly-logarithmic in $T$ and polynomial in $1/\epsilon$, where $\epsilon$ is the additive approximation error. Our algorithms are obtained respectively by using an $O(\log T)$-qubit semi-digital quantum encoding of the Brownian motion that allows for exponentiation of the stochastic process and by analyzing classical Monte Carlo algorithms inspired by the semi-digital encodings. The best quantum algorithm obtained using this approach has complexity $\widetilde{O}(1/\epsilon^{3})$ where the $\widetilde{O}$ suppresses factors poly-logarithmic in $T$ and $1/\epsilon$. The methods proposed in this work generalize to pricing options where the underlying asset price is modeled by a smooth function of a sub-Gaussian process and the payoff is dependent on the weighted time-average of the underlying asset price

The crosstalk between microbial sensors ELMO1 and NOD2 shape intestinal immune responses

ABSTRACTMicrobial sensors play an essential role in maintaining cellular homoeostasis. Our knowledge is limited on how microbial sensing helps in differential immune response and its link to inflammatory diseases. Recently we have confirmed that ELMO1 (Engulfment and Cell Motility Protein-1) present in cytosol is involved in pathogen sensing, engulfment, and intestinal inflammation. Here, we show that ELMO1 interacts with another sensor, NOD2 (Nucleotide-binding oligomerization domain-containing protein 2), that recognizes bacterial cell wall component muramyl dipeptide (MDP). The polymorphism of NOD2 is linked to Crohn’s disease (CD) pathogenesis. Interestingly, we found that overexpression of ELMO1 and mutant NOD2 (L1007fs) were not able to clear the CD-associated adherent invasive E. coli (AIEC-LF82). The functional implications of ELMO1-NOD2 interaction in epithelial cells were evaluated by using enteroid-derived monolayers (EDMs) from ELMO1 and NOD2 KO mice. Subsequently we also assessed the immune response in J774 macrophages depleted of either ELMO1 or NOD2 or both. The infection of murine EDMs with AIEC-LF82 showed higher bacterial load in ELMO1-KO, NOD2 KO EDMs, and ELMO1 KO EDMs treated with NOD2 inhibitors. The murine macrophage cells showed that the downregulation of ELMO1 and NOD2 is associated with impaired bacterial clearance that is linked to reduce pro-inflammatory cytokines and reactive oxygen species. Our results indicated that the crosstalk between microbial sensors in enteric infection and inflammatory diseases impacts the fate of the bacterial load and disease pathogenesis

The crosstalk between microbial sensors ELMO1 and NOD2 shape intestinal immune responses.

Microbial sensors play an essential role in maintaining cellular homoeostasis. Our knowledge is limited on how microbial sensing helps in differential immune response and its link to inflammatory diseases. Recently we have confirmed that ELMO1 (Engulfment and Cell Motility Protein-1) present in cytosol is involved in pathogen sensing, engulfment, and intestinal inflammation. Here, we show that ELMO1 interacts with another sensor, NOD2 (Nucleotide-binding oligomerization domain-containing protein 2), that recognizes bacterial cell wall component muramyl dipeptide (MDP). The polymorphism of NOD2 is linked to Crohn's disease (CD) pathogenesis. Interestingly, we found that overexpression of ELMO1 and mutant NOD2 (L1007fs) were not able to clear the CD-associated adherent invasive E. coli (AIEC-LF82). The functional implications of ELMO1-NOD2 interaction in epithelial cells were evaluated by using enteroid-derived monolayers (EDMs) from ELMO1 and NOD2 KO mice. Subsequently we also assessed the immune response in J774 macrophages depleted of either ELMO1 or NOD2 or both. The infection of murine EDMs with AIEC-LF82 showed higher bacterial load in ELMO1-KO, NOD2 KO EDMs, and ELMO1 KO EDMs treated with NOD2 inhibitors. The murine macrophage cells showed that the downregulation of ELMO1 and NOD2 is associated with impaired bacterial clearance that is linked to reduce pro-inflammatory cytokines and reactive oxygen species. Our results indicated that the crosstalk between microbial sensors in enteric infection and inflammatory diseases impacts the fate of the bacterial load and disease pathogenesis

Osteogenic Sarcoma of the Head and Neck: Is Chemotherapy Needed?

Head and neck osteosarcoma (HNOS) is a rare subtype of sarcoma that most commonly arises in the mandible or maxilla. Treatment for HNOS typically involves a multidisciplinary and multimodal approach depending on the size, grade, and histological subtype. Surgery by sarcoma-experienced head and neck surgeons and orthopedic oncologists remains a crucial component of treatment in all subtypes of HNOS, particularly for those with low-grade histology, which can be treated definitively with surgical resection if negative margins are obtained. Negative surgical margins are of utmost prognostic importance, and neoadjuvant or adjuvant radiation should be considered in patients with positive (or anticipated positive) margins/residual postoperative disease. Current data favors the use of (neo)adjuvant chemotherapy in patients with high-grade HNOS to improve overall survival but must be individualized to weigh benefits and risks of the short- and long-term effects of treatment. Our center uses a multidisciplinary treatment plan and notes anecdotal improvement in treatment outcomes with a combined surgical and ifosfamide-containing chemotherapeutic approach with radiotherapy for local control if positive margins. Large volume cohorts and adequate randomized control trials assessing the efficacy of chemotherapy in HNOS are scant and additional research and multi-institutional collaboration are needed to study polychemotherapeutic and radiation treatment regimens and outcomes more adequately

KIT resistance mutations identified by circulating tumor DNA and treatment outcomes in advanced gastrointestinal stromal tumor.

11514 Background: Tyrosine kinase inhibitors (TKIs) are the cornerstone treatment for advanced GIST via pharmacologic targeting of driver oncogenes such as KIT. Detection of KIT alterations through tissue-based next-generation sequencing (NGS) is common, but circulating tumor DNA (ctDNA)-based NGS is a less invasive alternative to identify driver and resistance mutations in advanced GIST. Patients (pts) with KIT-mutant GIST benefit from first-line (1L) imatinib; however, KIT resistance mutations may confer imatinib-resistance and differential sensitivity to subsequent TKIs. We sought to analyze ctDNA from GIST pts to determine whether certain resistance mutations were associated with superior outcomes with particular TKIs in the second-line and beyond (2L+). Methods: Under an approved institutional review board protocol, a retrospective analysis was performed with available ctDNA NGS results (Guardant360; Redwood City, CA) from pts (N = 104) who progressed on 1L imatinib between 2017-21. Using R statistical programming, we identified pts with primary KIT alterations (N = 64) and known resistance mutations in KIT exons 13 (N = 25) and 17 (N = 35). We studied the median time to treatment failure (mTTF), defined as the time from treatment start to treatment end (months) due to progressive disease or toxicity, for each 2L+ drug. Using Kaplan-Meier methods, we calculated Cox proportional-hazard ratios (HR) with confidence intervals (CI) and p-values for statistical significance. Results: 49% were male (median age 66; range, 31-94). Driver oncogenes were detected in 80% (N = 83), including KIT, NF1, PDGFRA and BRAF. Of those with a KIT alteration, 12 (19%) had KIT exon 9 mutations and 52 (81%) had KIT exon 11 mutations. KIT resistance mutations were observed in KIT exons 13 (N = 25; V654), 14 (N = 2; T670), and 17 (N = 45; D816, D820, N822, Y823). Pts with KIT resistance mutations received 2L+ therapy with avapritinib, dose-escalated imatinib, nilotinib, pazopanib, ponatinib, regorafenib, ripretinib, or sunitinib. mTTF for KIT exon 13 V654 pts treated with 2L+ sunitinib, imatinib 800mg, or other was 10.8, 7.5, and 3.7 months, respectively. TTF for sunitinib vs other 2L+ drugs showed a HR of 0.51 (CI 0.33-0.8), p = 0.003. mTTF for KIT exon 17 (non-V654) pts treated with 2L+ regorafenib, imatinib 800mg, or other was 4.6, 1.2, and 6.3 months, respectively. Comparison of mTTF for regorafenib vs other 2L+ drugs was not statistically significant. Conclusions: ctDNA is a noninvasive tool for detecting driver and resistance mutations in pts with advanced GIST. GIST pts with KIT exon 13 V654 resistance mutations had superior outcomes in the 2L+ setting with sunitinib. Regorafenib was not superior to other 2L+ TKIs in pts with KIT exon 17 resistance mutations, possibly due to their own activity against exon 17 resistance alterations. ctDNA-guided therapy warrants evaluation in a prospective clinical trial. </jats:p