Accuracy of portable ultrasound for obstetric biometry.

OBJECTIVE: We assessed the accuracy of two portable ultrasound machines (PUM) in obtaining fetal biometry and estimating gestational age. METHODS: We analyzed data from the Fetal Age Machine Learning Initiative, an observational study of pregnant women in the United States and Zambia. Each participant underwent assessment by an experienced sonographer using both a high-specification ultrasound machine (HSUM) and a PUM (either Butterfly iQ or Clarius C3) to measure fetal biometry and calculate estimated gestational age (EGA) at each visit. Through comparison of paired PUM-HSUM scans, we estimated agreement between individual biometry measurements and aggregate gestational age estimates by reporting mean difference, along with intraclass correlation coefficient (ICC) and Bland-Altman plots, adjusting for trend. RESULTS: 881 participants contributed 1386 paired PUM-HSUM ultrasound studies between April and December 2021. PUM studies included 991 Butterfly and 395 Clarius. Gestational age at scan ranged from 7 to 38 weeks. Compared to HSUM, the Butterfly PUM had a mean difference of -0.20 days (95%CI±0.40) in the 1st trimester and -0.68 days (95%CI±0.68) in the 2nd/3rd trimesters. Also compared to HSUM, the Clarius PUM had a mean difference of 0.47 days (95%CI±0.64) in the 1st trimester and -1.67 days (95%CI±0.43) in the 2nd/3rd trimesters. ICCs were 0.989 or greater throughout. Increasing gestational age was associated with increasing error and absolute error. Both PUM devices demonstrated a modest trend toward underestimation of EGA at advancing gestational ages in 2nd/3rd trimester scans, compared to HSUM. CONCLUSION: Both the Butterfly iQ and Clarius C3 PUM devices were highly accurate in performing fetal biometry in a diverse population from the US and Zambia. This article is protected by copyright. All rights reserved.

Increasing comparability among coral bleaching experiments.

Coral bleaching is the single largest global threat to coral reefs worldwide. Integrating the diverse body of work on coral bleaching is critical to understanding and combating this global problem. Yet investigating the drivers, patterns, and processes of coral bleaching poses a major challenge. A recent review of published experiments revealed a wide range of experimental variables used across studies. Such a wide range of approaches enhances discovery, but without full transparency in the experimental and analytical methods used, can also make comparisons among studies challenging. To increase comparability but not stifle innovation, we propose a common framework for coral bleaching experiments that includes consideration of coral provenance, experimental conditions, and husbandry. For example, reporting the number of genets used, collection site conditions, the experimental temperature offset(s) from the maximum monthly mean (MMM) of the collection site, experimental light conditions, flow, and the feeding regime will greatly facilitate comparability across studies. Similarly, quantifying common response variables of endosymbiont (Symbiodiniaceae) and holobiont phenotypes (i.e., color, chlorophyll, endosymbiont cell density, mortality, and skeletal growth) could further facilitate cross-study comparisons. While no single bleaching experiment can provide the data necessary to determine global coral responses of all corals to current and future ocean warming, linking studies through a common framework as outlined here, would help increase comparability among experiments, facilitate synthetic insights into the causes and underlying mechanisms of coral bleaching, and reveal unique bleaching responses among genets, species, and regions. Such a collaborative framework that fosters transparency in methods used would strengthen comparisons among studies that can help inform coral reef management and facilitate conservation strategies to mitigate coral bleaching worldwide.

Identification and characterisation of a platelet GPIb/V/IX-like complex on human breast cancers: implications for the metastatic process.

The glycoprotein (GP) Ib /V/IX receptor complex is an important adhesion molecule, originally thought to be unique to the megakaryocytic lineage. Recent evidence now indicates that GPIb /V/IX may be more widely expressed. In this study we report the presence of all subunits of the complex on four breast cancer cell lines, and 51 / 80 primary breast tumours. The surface expression of GPIb /V/IX was confirmed by flow cytometry, and by immunoprecipitation of biotin surface-labelled tumour cells. Western blotting of cell lysates under reducing conditions revealed that tumour cell-GPIb alpha had a relative molecular weight of 95 kDa as compared to 135 kDa on platelets. Despite the discrepant protein size, molecular analyses on the tumour cell-GPIb alpha subunit using RT-PCR and DNA sequencing revealed 100% sequence homology to platelet GPIb alpha. Tumour cell-GPIb /V/IX was capable of binding human von Willebrand factor (vWf), and this binding caused aggregation of tumour cells in suspension. Tumour cells bound to immobilised vWf in the presence of EDTA and demonstrated prominent filapodial extensions indicative of cytoskeletal reorganisation. Furthermore, in a modified Boyden chamber assay, prior exposure to vWf or a GPIb alpha monoclonal antibody, AK2, enhanced cell migration. The presence of a functional GPIb /V/IX-like complex in tumour cells suggests that this complex may participate in the process of haematogenous breast cancer metastasis.

Epidermal growth factor promotes MDA-MB-231 breast cancer cell migration through a phosphatidylinositol 3'-kinase and phospholipase C-dependent mechanism.

Epidermal growth factor receptor (EGFR) levels predict a poor outcome in human breast cancer and are most commonly associated with proliferative effects of epidermal growth factor (EGF), with little emphasis placed on motogenic responses to EGF. We found that MDA-MB-231 human breast cancer cells elicited a potent chemotactic response despite their complete lack of a proliferative response to EGF. Antagonists of EGFR ligation, the EGFR kinase, phosphatidylinositol 3'-kinase, and phospholipase C, but not the mitogen-activated protein kinases (extracellular signal-regulated protein kinase 1 and 2), blocked MDA-MB-231 chemotaxis. These findings suggest that EGF may influence human breast cancer progression via migratory pathways, the signaling for which appears to be dissociated, at least in part, from the proliferative pathways.

The biochemistry of cancer dissemination.

The progression of a tumor cell from one of benign delimited proliferation to invasive and metastatic growth is the major cause of poor clinical outcome of cancer patients. Recent research has revealed that this complex process requires many components for successful dissemination and growth of the tumor cell at secondary sites. These include angiogenesis, enhanced extracellular matrix degradation via tumor and host-secreted proteases, tumor cell migration, and modulation of tumor cell adhesion. Each individual component is multifaceted and is discussed within this review with respect to historical and recent findings. The identification of components and their interrelationship have yielded new therapeutic targets leading to the development of agents that may prove effective in the treatment of cancer and its metastatic progression.

Epidermal growth factor (EGF) increases the in vitro invasion, motility and adhesion interactions of the primary renal carcinoma cell line, A704.

Metastasis is a multistep process that involves alterations in a tumour cell's invasion, motility and adhesive capabilities. This study examined the effect of EGF on the in vitro invasion, motility and adhesion of the primary renal adenocarcinoma cell line, A704. Stimulation of the tumour cells by EGF (40 ng/ml) for a period of 24 h increased the in vitro invasion (P = 0.040) and motility (P = 0.039). Cell adhesion was examined on fibronectin, laminin, collagen IV and a 1:1:1 mix of the three extracellular matrix components. After EGF (40 ng/ml) stimulation, adhesion was significantly decreased on fibronectin (P = 0.022) and collagen type IV (P = 0.026), but increased on the 1:1:1 mix of extracellular matrix components (P = 0.022). The 92 kDa matrix metalloproteinase (MMP-9) present in the cell-conditioned medium was also increased after a 24 h stimulation with EGF (40 ng/ml) when measured. Hence, EGF can modulate the in vitro invasion, motility, adhesiveness and matrix metalloproteinase production in the A704 cell line, and subsequently may have a role in the metastatic potential of some renal carcinomas.

Tumor induction by Cryptococcus neoformans.

A human isolate of Cryptococcus neoformans strain CIA, which was originally obtained in 1963, produced fatal disease in mice. Postmortem examinations showed extensive central nervous system disease. After using this yeast for research for 7 years, we found that it began to produce large tumors after intraperitoneal inoculation in mice. The present study showed that the tumors consisted of large agglomerates of yeast cells, capillaries, and reticular stroma. In concomitant experiments, the same C. neoformans strain, introduced into the lungs of mice in an aerosol, produced asymptomatic infections. A definition for the term "cryptococcoma" is proposed.