Query Augmentation Using Search Engine Results to Improve Answers Generated by Large Language Models

Large Language Model (LLM) and Generative Pre-trained Transformer (GPT) technology has the ability to generate responses to questions provided in text format. While such technology produces text content with plausible answers to a given question, it is difficult to judge the trustworthiness of the generated answers. It has been shown that answers generated by such technology may not always be factually accurate. This disclosure describes automated techniques to improve the credibility and confidence of machine-generated answers by using results from a search engine. Per the techniques, search results corresponding to a user input query are used to generate an augmented query that is provided as input to an LLM. Such augmentation adds context and can improve the quality and reliability of answers generated by the LLM. Further, the techniques can also be utilized to add citations to the generated answer and to indicate a confidence level in the generated answer

Edit Distance based RL for RNNT decoding

RNN-T is currently considered the industry standard in ASR due to its exceptional WERs in various benchmark tests and its ability to support seamless streaming and longform transcription. However, its biggest drawback lies in the significant discrepancy between its training and inference objectives. During training, RNN-T maximizes all alignment probabilities by teacher forcing, while during inference, it uses beam search which may not necessarily find the maximum probable alignment. Additionally, RNN-T's inability to experience mistakes during teacher forcing training makes it more problematic when a mistake occurs in inference. To address this issue, this paper proposes a Reinforcement Learning method that minimizes the gap between training and inference time. Our Edit Distance based RL (EDRL) approach computes rewards based on the edit distance, and trains the network at every action level. The proposed approach yielded SoTA WERs on LibriSpeech for the 600M Conformer RNN-T model.Comment: 5 pages, 2 figure

Management of an elderly patient with respiratory failure due to double aortic arch

AbstractVascular rings are congenital malformations of the aortic arch. A double aortic arch (DAA), the most common type of vascular ring, results from the failure of the fourth embryonic branchial arch to regress, leading to an ascending aorta that divides into a left and right arch that fuse together to completely encircle the trachea and esophagus. The subsequent DAA causes compressive effects on the trachea and esophagus that typically manifests in infancy or early childhood. Adult presentations, particularly in the elderly, are exceedingly rare. Historically such patients have a long-standing history of dyspnea on exertion and dysphagia, with many assumed to have obstructive lung or intrinsic cardiac disease. We describe a case of an elderly woman who presented with respiratory failure due to DAA. In her case, surgery was not feasible and we describe our experience with airway stenting

Specific Inhibition of Soluble γc Receptor Attenuates Collagen-Induced Arthritis by Modulating the Inflammatory T Cell Responses

IL-17 produced by Th17 cells has been implicated in the pathogenesis of rheumatoid arthritis (RA). It is important to prevent the differentiation of Th17 cells in RA. Homodimeric soluble γc (sγc) impairs IL-2 signaling and enhances Th17 differentiation. Thus, we aimed to block the functions of sγc by inhibiting the formation of homodimeric sγc. The homodimeric form of sγc was strikingly disturbed by sγc-binding DNA aptamer. Moreover, the aptamer effectively inhibited Th17 cell differentiation and restored IL-2 and IL-15 signaling impaired by sγc with evidences of increased survival of T cells. sγc was highly expressed in SF of RA patients and increased in established CIA mice. The therapeutic effect of PEG-aptamer was tested in CIA model and its treatment alleviated arthritis pathogenesis with impaired differentiation of pathogenic Th17, NKT1, and NKT17 cells in inflamed joint. Homodimeric sγc has pathogenic roles to exacerbate RA progression with differentiation of local Th17, NKT1, and NKT17 cells. Therefore, sγc is suggested as target of a therapeutic strategy for RA

A rare presentation of pulmonary sarcoidosis as a solitary lung mass: a case report

Abstract Background Sarcoidosis is a multisystem, chronic granulomatous disease of unknown etiology that predominantly affects the lungs. Pulmonary sarcoidosis classically presents with constitutional symptoms and computed tomographic scan findings of bilateral, symmetric micronodules in a peribronchovascular distribution with upper and middle lung zone predominance accompanied by bilateral, symmetric hilar lymphadenopathy. A solitary lung mass is a rare finding for pulmonary sarcoidosis, and with its associated constitutional symptoms, it strongly mimics a malignancy. We aimed to provide further insight into the broad differential diagnosis of a lung mass by describing our experiences in the care of a patient who presented with clinical and radiographic features of lung cancer who was ultimately found to have an atypical manifestation of stage II pulmonary sarcoidosis. Case presentation A 44-year-old African American woman with a history of childhood asthma and type 2 diabetes mellitus presented with shortness of breath. After being treated for a presumed asthma exacerbation with prednisone, she experienced worsening dyspnea, night sweats, and unintentional weight loss. Further evaluation revealed a large left lower lobe mass and hilar lymphadenopathy. A computed tomography-guided biopsy of the lung mass revealed a multifocal non-necrotizing granuloma with multinucleated giant cells. Although consistent with sarcoidosis, this finding could represent a sarcoid-like reaction secondary to an occult malignancy. A more extensive repeat biopsy via bronchoscopy and mediastinoscopy revealed granulomatous inflammation without evidence of malignancy or infection. These procedures confirmed the diagnosis of pulmonary sarcoidosis, and she was started on treatment with high-dose prednisone. Her treatment course was complicated by hyperglycemia necessitating insulin therapy, but after 3 months of therapy, she reported improvement in her dyspnea, and repeat imaging revealed a significant decrease in the size of the lung mass and lymphadenopathy. Given her clinical and radiographic response, she was continued on a prednisone taper. Conclusions Atypical manifestations of pulmonary sarcoidosis are diagnostically challenging because the clinical and radiographic features of the disease mimic those of a malignancy. We aimed to illustrate a unique etiology of a lung mass and the importance of maintaining a broad differential diagnosis. Nonetheless, with the possibility of a malignancy, a high index of suspicion is necessary for timely diagnosis and optimal management

Macrophage-derived PDGF-B induces muscularization in murine and human pulmonary hypertension

Excess macrophages and smooth muscle cells (SMCs) characterize many cardiovascular diseases, but crosstalk between these cell types is poorly defined. Pulmonary hypertension (PH) is a lethal disease in which lung arteriole SMCs proliferate and migrate, coating the normally unmuscularized distal arteriole. We hypothesized that increased macrophage platelet-derived growth factor–B (PDGF-B) induces pathological SMC burden in PH. Our results indicate that clodronate attenuates hypoxia-induced macrophage accumulation, distal muscularization, PH, and right ventricle hypertrophy (RVH). With hypoxia exposure, macrophage Pdgfb mRNA was upregulated in mice, and LysM‑Cre mice carrying floxed alleles for hypoxia-inducible factor 1a, hypoxia-inducible factor 2a, or Pdgfb had reduced macrophage Pdgfb and were protected against distal muscularization and PH. Conversely, LysM‑Cre von-Hippel Lindaufl/fl mice had increased macrophage Hifa and Pdgfb and developed distal muscularization, PH, and RVH in normoxia. Similarly, Pdgfb was upregulated in macrophages from human idiopathic or systemic sclerosis–induced pulmonary arterial hypertension patients, and macrophage-conditioned medium from these patients increased SMC proliferation and migration via PDGF-B. Finally, in mice, orotracheal administration of nanoparticles loaded with Pdgfb siRNA specifically reduced lung macrophage Pdgfb and prevented hypoxia-induced distal muscularization, PH, and RVH. Thus, macrophage-derived PDGF-B is critical for pathological SMC expansion in PH, and nanoparticle-mediated inhibition of lung macrophage PDGF-B has profound implications as an interventional strategy for PH