View adaptive unified self-supervised technique for abdominal organ segmentation.

Automatic abdominal organ segmentation is an essential prerequisite for accurate volumetric analysis, disease diagnosis, and tracking by medical practitioners. However, the deformable shapes, variable locations, overlapping with nearby organs, and similar contrast make the segmentation challenging. Moreover, the requirement of a large manually labeled dataset makes it harder. Hence, a semi-supervised contrastive learning approach is utilized to perform the automatic abdominal organ segmentation. Existing 3D deep learning models based on contrastive learning are not able to capture the 3D context of medical volumetric data along three planes/views: axial, sagittal, and coronal views. In this work, a semi-supervised view-adaptive unified model (VAU-model) is proposed to make the 3D deep learning model as view-adaptive to learn 3D context along each view in a unified manner. This method utilizes the novel optimization function that assists the 3D model to learn the 3D context of volumetric medical data along each view in a single model. The effectiveness of the proposed approach is validated on the three types of datasets: BTCV, NIH, and MSD quantitatively and qualitatively. The results demonstrate that the VAU model achieves an average Dice score of 81.61% which is a 3.89% improvement compared to the previous best results for pancreas segmentation in multi-organ dataset BTCV. It also achieves an average Dice score of 77.76% and 76.76% for the pancreas under the single organ non-pathological NIH dataset, and pathological MSD dataset.

PI3K signaling specifies proximal-distal fate by driving a developmental gene regulatory network in SOX9+ mouse lung progenitors.

The tips of the developing respiratory buds are home to important progenitor cells marked by the expression of SOX9 and ID2. Early in embryonic development (prior to E13.5), SOX9+progenitors are multipotent, generating both airway and alveolar epithelium, but are selective progenitors of alveolar epithelial cells later in development. Transcription factors, including Sox9, Etv5, Irx, Mycn, and Foxp1/2 interact in complex gene regulatory networks to control proliferation and differentiation of SOX9+progenitors. Molecular mechanisms by which these transcription factors and other signaling pathways control chromatin state to establish and maintain cell-type identity are not well-defined. Herein, we analyze paired gene expression (RNA-Seq) and chromatin accessibility (ATAC-Seq) data from SOX9+ epithelial progenitor cells (EPCs) during embryonic development in Mus musculus. Widespread changes in chromatin accessibility were observed between E11.5 and E16.5, particularly at distal cis-regulatory elements (e.g. enhancers). Gene regulatory network (GRN) inference identified a common SOX9+ progenitor GRN, implicating phosphoinositide 3-kinase (PI3K) signaling in the developmental regulation of SOX9+ progenitor cells. Consistent with this model, conditional ablation of PI3K signaling in the developing lung epithelium in mouse resulted in an expansion of the SOX9+ EPC population and impaired airway epithelial cell differentiation. These data demonstrate that PI3K signaling is required for epithelial patterning during lung organogenesis, and emphasize the combinatorial power of paired RNA and ATAC seq in defining regulatory networks in development.

Studying how lungs develop has helped us understand and treat often-devastating lung diseases. This includes diseases like cystic fibrosis which result from spelling mistakes known as mutations in a person's genetic code. However, not all lung diseases involve mutations. Many other diseases, in both adults and children, are caused by genes failing to switch on or off at some point during lung development. DNA is surrounded by various proteins which package it into a compressed structure known as chromatin. Cells can control which genes are turned on or off by modifying how tightly packed parts of the genetic code are within chromatin. Changes in chromatin accessibility, also known as 'epigenetic' changes, are a normal part of development, and guide cells towards specific jobs or identities as an organ matures. However, how this happens in the developing lung is poorly understood. Here, Khattar, Fernandes et al. set out to determine how chromatin accessibility shapes development of the tissue lining the lungs, focusing on a group of progenitor cells which produce the protein SOX9. These cells are initially found at the tips of the early lung, where they go on to develop into the cells that line the whole of the mature organ. Initial experiments used large-scale genetic techniques to measure gene activity and chromatin accessibility simultaneously in progenitor cells extracted from the lungs of mice. Khattar, Fernandes et al. were then able to predict the signaling pathways that shape the lung lining based on which genes were surrounded by unpacked chromatin, and determine the proteins responsible for these epigenetic changes. This included the signaling pathway Phosphatidylinositol 3 kinase (PI3K) which is involved in a number of cellular processes. Additional experiments in mice confirmed that the PI3K pathway became active very early in lung development and remained so until adulthood. In contrast, mice lacking a gene that codes for a key part of the PI3K pathway had defective lungs which failed to develop a proper lining. The data generated in this study will provide an important resource for future studies investigating how epigenetic changes drive normal lung development. Khattar, Fernandes et al. hope that this knowledge will help researchers to better understand the cause of human lung diseases, and identify already available 'epigenetic drugs' which could be repurposed to treat them.

Recurrent ovarian malignancy presenting as cutaneous metastasis.

Cutaneous metastasis from ovarian carcinoma is relatively uncommon in clinical practice. We report the case of the woman who presented to us with clitoral nodules and skin nodules. Histopathological examination of nodules confirmed the diagnosis of metastasis of an ovarian carcinoma. Despite poor prognosis, the patient responded and survived well beyond the expected four months survival of similar cases.

'Padhar regime' - a low-dose magnesium sulphate treatment for eclampsia.

AIMS: To determine the recurrent convulsion rate using low-dose magnesium sulphate regime in eclampsia and to identify toxicity and complications with clinical parameters. METHODS: Prospective study with two different magnesium sulphate regimes in two slightly clinically different subgroups. Group A that came directly to our hospital and group B who had already received an injection of diazepam or Phenergan at the referring hospital. Group A received 10 g and group B 6 g loading dose of magnesium sulphate. Both groups received 4 g maintenance dose every 4 h. RESULTS: Out of 95 eclamptic patients, only one woman in group B had recurrent convulsion. All women maintained normal respiratory rates. 39 (41.1%) women had absent knee jerks on at least one occasion when the maintenance dose was omitted. Urinary output was more than 30 ml/h in 92 (96.8%) women. In 5 women, maintenance dose had to be augmented to 5 g as reflexes were exaggerated. CONCLUSION: The low-dose regime appears to control and prevent convulsions effectively in Indian women. Clinical monitoring appears to be sufficient. We hope to be able to reassure health professionals at primary and secondary level hospitals about the safety of magnesium.