A comparative study of histotripsy parameters for the treatment of fibrotic ex-vivo human benign prostatic hyperplasia tissue.

Histotripsy is a noninvasive focused ultrasound therapy that mechanically fractionates tissue to create well-defined lesions. In a previous clinical pilot trial to treat benign prostatic hyperplasia (BPH), histotripsy did not result in consistent objective improvements in symptoms, potentially because of the fibrotic and mechanically tough nature of this tissue. In this study, we aimed to identify the dosage required to homogenize BPH tissue by different histotripsy modalities, including boiling histotripsy (BH) and cavitation histotripsy (CH).

A customizable secure DIY web application for accessing, sharing, and browsing aggregate experimental results and metadata.

Summary: A problem spanning across many research fields is that processed data and research results are often scattered, which makes data access, analysis, extraction, and team sharing more challenging. We have developed a platform for researchers to easily manage tabular data with features like browsing, bookmarking, and linking to external open knowledge bases. The source code, originally designed for genomics research, is customizable for use by other fields or data, providing a no- to low-cost DIY system for research teams.

A Comparative Study of Histotripsy Parameters for the Treatment of Fibrotic ex-vivo Human Benign Prostatic Hyperplasia Tissue.

Histotripsy is a noninvasive focused ultrasound therapy that mechanically fractionates tissue to create well-defined lesions. In a previous clinical pilot trial to treat benign prostatic hyperplasia (BPH), histotripsy did not result in consistent objective improvements in symptoms, potentially because of the fibrotic and mechanically tough nature of this tissue. In this study, we aimed to identify the dosage required to homogenize BPH tissue by different histotripsy modalities, including boiling histotripsy (BH) and cavitation histotripsy (CH).

Mycobacterium tuberculosis resides in lysosome-poor monocyte-derived lung cells during chronic infection.

Mycobacterium tuberculosis (Mtb) infects lung myeloid cells, but the specific Mtb-permissive cells and host mechanisms supporting Mtb persistence during chronic infection are incompletely characterized. We report that after the development of T cell responses, CD11clo monocyte-derived cells harbor more live Mtb than alveolar macrophages (AM), neutrophils, and CD11chi monocyte-derived cells. Transcriptomic and functional studies revealed that the lysosome pathway is underexpressed in this highly permissive subset, characterized by less lysosome content, acidification, and proteolytic activity than AM, along with less nuclear TFEB, a regulator of lysosome biogenesis.

Mycobacterium tuberculosis resides in lysosome-poor monocyte-derived lung cells during chronic infection.

(Mtb) persists in lung myeloid cells during chronic infection. However, the mechanisms allowing Mtb to evade elimination are not fully understood. Here, we determined that in chronic phase, CD11c monocyte-derived lung cells termed MNC1 (mononuclear cell subset 1), harbor more live Mtb than alveolar macrophages (AM), neutrophils, and less permissive CD11c MNC2.

resides in lysosome-poor monocyte-derived lung cells during chronic infection.

(Mtb) infects cells in multiple lung myeloid cell subsets and causes chronic infection despite innate and adaptive immune responses. However, the mechanisms allowing Mtb to evade elimination are not fully understood. Here, using new methods, we determined that after T cell responses have developed, CD11c monocyte-derived lung cells termed MNC1 (mononuclear cell subset 1), harbor more live Mtb compared to alveolar macrophages (AM), neutrophils, and less permissive CD11c MNC2.

Physical Activity as a Predictor of Chronic Pain Following Pediatric Spinal Surgery.

Objectives: (1) Characterize objective physical activity patterns via actigraphy over 4 months postspinal fusion surgery, and (2) examine associations between activity patterns at 2-week and chronic postsurgical pain (CPSP) status at 4 months.

Materials And Methods: Data from 109 youth (10 to 18 y) who underwent spinal fusion surgery at a children's hospital in the Northwestern United States were analyzed. Youth completed questionnaires and actigraphic assessment of physical activity presurgery, and 2 weeks and 4 months postsurgery.

Psychosocial Predictors of Acute and Chronic Pain in Adolescents Undergoing Major Musculoskeletal Surgery.

Acute and chronic pain delay recovery and impair outcomes after major pediatric surgery. Understanding unique risk factors for acute and chronic pain is critical to developing effective treatments for youth at risk. We aimed to identify adolescent and family psychosocial predictors of acute and chronic postsurgical pain after major surgery in adolescents.

A Review of Recent Advances in Ultrasound, Placed in the Context of Pain Diagnosis and Treatment.

Ultrasound plays a significant role in the diagnosis and treatment of pain, with significant literature reaching back many years, especially with regard to diagnostic ultrasound and its use for guiding needle-based delivery of drugs. Advances in ultrasound over at least the last decade have opened up new areas of inquiry and potential clinical efficacy in the context of pain diagnosis and treatment. Here we offer an overview of the recent literature associated with ultrasound and pain in order to highlight some promising frontiers at the intersection of these two subjects.

Innate and ozone-induced airway hyperresponsiveness in obese mice: role of TNF-α.

Innate airway hyperresponsiveness (AHR) and augmented responses to ozone, an asthma trigger, are characteristics of obese mice. Systemic inflammation, a condition of increased circulating concentrations of inflammatory moieties, occurs in obesity. We hypothesized that TNF-α, via its effects as a master effector of this systemic inflammation, regulates innate AHR and augmented responses to ozone in obese mice.

γδ T cells are required for pulmonary IL-17A expression after ozone exposure in mice: role of TNFα.

Ozone is an air pollutant that causes pulmonary symptoms. In mice, ozone exposure causes pulmonary injury and increases bronchoalveolar lavage macrophages and neutrophils. We have shown that IL-17A is important in the recruitment of neutrophils after subacute ozone exposure (0.

Augmented pulmonary responses to acute ozone exposure in obese mice: roles of TNFR2 and IL-13.

Background: Acute ozone (O(3)) exposure results in greater inflammation and airway hyperresponsiveness (AHR) in obese versus lean mice.

Objectives: We examined the hypothesis that these augmented responses to O(3) are the result of greater signaling through tumor necrosis factor receptor 2 (TNFR2) and/or interleukin (IL)-13.

Methods: We exposed lean wild-type (WT) and TNFR2-deficient (TNFR2(-/-)) mice, and obese Cpe(fat) and TNFR2-deficient Cpe(fat) mice (Cpe(fat)/TNFR2(-/-)), to O(3) (2 ppm for 3 hr) either with or without treatment with anti-IL-13 or left them unexposed.

Role of TNFR1 in the innate airway hyperresponsiveness of obese mice.

The purpose of this study was to examine the role of tumor necrosis factor receptor 1 (TNFR1) in the airway hyperresponsiveness characteristic of obese mice. Airway responsiveness to intravenous methacholine was measured using the forced oscillation technique in obese Cpe(fat) mice that were either sufficient or genetically deficient in TNFR1 (Cpe(fat) and Cpe(fat)/TNFR1(-/-) mice) and in lean mice that were either sufficient or genetically deficient in TNFR1 [wild-type (WT) and TNFR1(-/-) mice]. Compared with lean WT mice, Cpe(fat) mice exhibited airway hyperresponsiveness.

Obesity and airway responsiveness: role of TNFR2.

Obese mice exhibit innate airway hyperresponsiveness (AHR), a feature of asthma. Tumor necrosis factor alpha (TNFα) is implicated in the disease progression and chronic inflammatory status of both obesity and asthma. TNF acts via two TNF receptors, TNFR1 and TNFR2.

Impact of aging on pulmonary responses to acute ozone exposure in mice: role of TNFR1.

Context: Chamber studies in adult humans indicate reduced responses to acute ozone with increasing age. Age-related changes in TNFα have been observed. TNFα induced inflammation is predominantly mediated through TNFR1.