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Three versions of syncytiotrophoblast exist in the human placenta: an invasive type associated with the implanting conceptus, non-invasive villous type of definitive placenta, and placental bed giant cells. Syncytins are encoded by modified env genes of endogenous retroviruses (ERV), but how they contribute functionally to placental syncytial structures is unclear. A minimum of eight genes (ERVW1, ERVFRD-1, ERVV-1, ERVV-2, ERVH48-1, ERVMER34-1, ERV3-1, & ERVK13-1) encoding syncytin family members are expressed in human trophoblast, the majority from implantation to term. ERVW1 (Syncytin 1) and ERVFRD-1 (Syncytin 2) are considered the major fusogens, but, when the expression of their genes is analyzed by single cell RNAseq in first trimester placenta, their transcripts are distinctly patterned and also differ from those of their proposed binding partners, SLC1A5 and MFSD2A, respectively. ERVRH48-1 (suppressyn or SUPYN) and ERVMER34-1 are probable negative regulators of fusion and co-expressed, primarily in cytotrophoblast. The remaining genes and their products have been little studied. Syncytin expression is a feature of placental development in almost all eutherian mammals studied, in at least one marsupial, and in viviparous lizards, which lack the trophoblast lineage. Their expression has been inferred to be essential for pregnancy success in the mouse. All the main human ERV genes arose following independent retroviral insertion events, none of which trace back to the divergence of eutherians and metatherians (marsupials). While syncytins may be crucial for placental development, it seems unlikely that they helped orchestrate the divergence of eutherians and marsupials., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Introduction: Inflammation and infection, including dental infectious diseases, are factors that can induce preterm birth. We previously reported that mice with dental Porphyromonas gingivalis infection could be used as a model of preterm birth. In this model, cyclooxygenase (COX)-2 and interleukin (IL)-1β levels are increased, and P. gingivalis colonies are observed in the fetal membrane. However, the mechanism underlying fetal membrane inflammation remains unknown. Therefore, we investigated the immune responses of human amnion to P. gingivalis in vitro., Methods: Epithelial and mesenchymal cells were isolated from human amnion using trypsin and collagenase, and primary cell cultures were obtained. Confluent cells were stimulated with P. gingivalis lipopolysaccharide (P.g-LPS) or P. gingivalis. mRNA expressions of IL-1β, IL-8, IL-6 and COX-2, protein expressions of nuclear factor (NF)-κB pathway components and culture medium levels of prostaglandin E 2 were evaluated., Results: Following stimulation with 1 μg/mL P.g-LPS, the mRNA expression levels of IL-1β, IL-8, IL-6 and COX-2 in mesenchymal cells were increased 5.9-, 3.3-, 4.2- and 3.1-fold, respectively. Similarly, the expression levels of IL-1β, IL-8, IL-6 and COX-2 in mesenchymal cells were increased by 7.6-, 8.2-, 13.4- and 9.3-fold, respectively, after coculture with P. gingivalis. Additionally, stimulation with P.g-LPS or P. gingivalis resulted in the activation of NF-κB signaling and increased production of IL-1β and prostaglandin E 2 . In contrast, no significant changes were observed in epithelial cells., Discussion: Our findings suggest that mesenchymal cells might mediate the inflammatory responses to P. gingivalis and P.g-LPS, thereby producing inflammation that contributes to the induction of preterm birth., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

The anatomy of aortic great vessels is relevant in surgeries of the anterior neck, especially with a tracheostomy, thyroidectomy, or mediastinoscopy. Variations in their anatomy could lead to severe complications if not recognized. An aberrant high-riding innominate artery incidentally encountered during mediastinoscopy is presented.

The MHB-2 cell line, established from a mouse hepatoblastoma (HB), was subjected to the reverse transcriptase-polymerase chain reaction (RT-PCR) for evaluation of gene expression related to cell differentiation. RNAs for c-kit, CD34, thy-1, albumin, cytokeratin (CK) 8, 18 and 19 could be detected, but expression of alpha-fetoprotein, glucose-6-phosphatase, tyrosine aminotransferase and CK7 was not observed. MHB-2 cells were positive for CK8/18 but negative for c-kit, CD34, thy-1 and albumin on protein level. Immunohistochemical staining of the HB in vivo revealed diffusely expressed c-kit. Thy-1-positive HB cells were sparsely observed, but the tumor was negative for CD34 and rarely positive for CK8/18. By in situ hybridization, the HB was positive for CK18 but negative for CK19. Slight expression of albumin, but the lack of immature hepatocytic marker suggested some heterogeneous hepatocyte or an undifferentiated cell from other origin. Furthermore, positive expression of CK19 as well as CK8 and CK18 in culture strongly suggested the differentiation into a biliary lineage or the bidirectional state. In conclusion, the present study indicated the mouse HB to have de-differentiated, bipotent, or biliary-like cell characteristics, and considering the histological difference between HB and biliary tumors, it suggests the mouse HB cells are closely like some sort of hepatic undifferentiated cells.

This chapter argues that a basal ganglia-brainstem system throughout the mesopontine tegmentum contributes to an automatic control of movement that operates in conjunction with voluntary control processes. Activity of a muscle tone inhibitory system and the locomotion executing system can be steadily balanced by a net excitatory cortical input and a net inhibitory basal ganglia input to these systems. We further propose that dysfunction of the basal ganglia-brainstem system, together with that of the cortico-basal ganglia loop, underlies the pathogenesis of motor disturbances expressed in basal ganglia diseases.

We report on a boy with normal mental development who had muscle hypotonia and congenital dislocation of the hip and knee joints. Histochemical and biochemical examinations of his muscle specimen revealed no succinate dehydrogenase (SDH) activity. Since the NADH cytochrome c reductase and cytochrome c oxidase activities were normal, we concluded that he had an isolated SDH deficiency. Our patient provides further evidence for the clinical variability of this disorder.

We investigated DNA damage induced by aminoacetone, a metabolite of threonine and glycine. Pulsed-field gel electrophoresis revealed that aminoacetone caused cellular DNA cleavage. Aminoacetone increased the amount of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in human cultured cells in a dose-dependent manner. The formation of 8-oxodG in calf thymus DNA increased due to aminoacetone only in the presence of Cu(II). DNA ladder formation was observed at higher concentrations of aminoacetone than those causing DNA cleavage. Flow cytometry showed that aminoacetone enhanced the generation of hydrogen peroxide (H2O2) in cultured cells. Aminoacetone caused damage to 32P-5'-end-labeled DNA fragments, obtained from the human c-Ha-ras-1 and p53 genes, at cytosine and thymine residues in the presence of Cu(II). Catalase and bathocuproine inhibited DNA damage, suggesting that H2O2 and Cu(I) were involved. Analysis of the products generated from aminoacetone revealed that aminoacetone underwent Cu(II)-mediated autoxidation in two different pathways: the major pathway in which methylglyoxal and NH+4 are generated and the minor pathway in which 2,5-dimethylpyrazine is formed through condensation of two molecules of aminoacetone. These findings suggest that H2O2 generated by the autoxidation of aminoacetone reacts with Cu(I) to form reactive species capable of causing oxidative DNA damage., (Copyright 1999 Academic Press.)

Lung herniation after thoracotomy is rare. We report a 66-year-old man who presented with this complication after undergoing attempted minimally invasive direct coronary artery bypass grafting. The defect was repaired with a composite of Marlex mesh and methyl methacrylate.

Preliminary data indicate that positron emission tomography (PET) following injection of fluorodeoxyglucose F18 (FDG) is sensitive and specific for detecting malignant cells in chest tumors and mediastinal lymph nodes. We report a case of non-small cell lung cancer metastatic to clinically normal scalene lymph nodes that was correctly staged by FDG-PET.

Positron emission tomography detects increased glucose uptake in malignant tissue using the glucose analogue [2-18F]fluoro-2-deoxy-D-glucose. We reviewed the scans obtained in 62 patients with lung tumors. All had undergone computed tomography and had tissue-based diagnoses: 22 had adenocarcinomas, 12 had squamous cell carcinomas, 13 had other malignancies, 1 had organizing pneumonia, 1 had a hamartoma, and 13 had granulomas. Positron emission tomography with [2-18F]fluoro-2-deoxy-D-glucose identified 44 of 47 malignancies. Two of three false-negative findings were tumors that were 1 cm2 or less and the other was a bronchioloalveolar carcinoma. All three false-positive findings were granulomas. The sensitivity and specificity of the technique were 93.6% and 80%, respectively, and the positive and negative predictive values were 93.6% and 80%, respectively. The differential uptake ratio was determined in all 62 patients. The mean differential uptake ratio (+/- the standard error of the mean) for malignant tumors was 6.4 +/- 0.56 and that for benign tumors was 1.14 +/- 0.26 (p < 0.0001, t test). Twenty-five of the patients had N2 lymph nodes evaluated pathologically. Positron emission tomography with [2-18F]fluoro-2-deoxy-D-glucose identified negative N2 nodes in 19 of 22 patients (86%) with negative nodes and positive N2 nodes in 2 of 3 patients (66%) with positive nodes, including one instance missed by computed tomography.(ABSTRACT TRUNCATED AT 250 WORDS)

A case in which a retrograde cardioplegia catheter was inserted into the coronary sinus for retrieval of antegrade cardioplegia in a patient with chronic renal failure is described. Potassium levels were maintained within normal limits throughout the procedure.

Although the term implies a persistent communication through which fluid might drain, how a pericardial window works is not clear. We believe that the mechanism of success is not window but rather fusion of the epicardium to the pericardium with obliteration of the potential space. To evaluate this, we studied 28 patients, all of whom underwent a subxiphoid pericardial window procedure with tube drainage maintained until output was minimal. There were no operative deaths, and 26 patients (92.9%) obtained permanent relief. Postoperative echocardiograms demonstrated thickening of the pericardium/epicardium and obliteration of the pericardial space. Autopsy performed on 4 patients who died of their underlying malignancy confirmed this fusion, which begins as an inflammatory process. A subxiphoid pericardial window relieves effusions with a low operative mortality and good long-term success (92.9%, 26 of 28). This success is dependent on the inflammatory fusion of the epicardium to pericardium and not maintenance of a window. Tube decompression should be maintained until fluid output is minimal to allow apposition and fusion of the two surfaces.

The purpose of this study was to determine the feasibility of using the pericardium as a source of endothelial cells. Nineteen pieces of fresh pericardium were obtained from nine mongrel dogs. Cells were prepared by collagenase digestion of the pericardium for 24 minutes followed by centrifugation. The cells were divided into three groups: The supernatant subjected to no further steps, Group I (N = 6); filtration through a 15 micron porous mesh, Group II (N = 6); and Percoll gradient separation with medium 199, Group III (N = 7). The cells obtained were cultured for seven days in tissue culture media. Yield (cells x 10(5)/gram fresh tissue) was determined with Methods I, II, and III, producing 32.4 +/- 25.9 (SD), 0.96 +/- 0.6 and 0.57 +/- 0.5, respectively (I vs II or III, p less than 0.01). Fibroblast contamination determined by phase contrast light microscopy was demonstrated in 6/6 cultures with Method I, 3/6 with II and 1/7 for III (I vs III, p less than 0.01). An assay for endothelial cells (Factor VIII) was positive in 2/6 cultures with Method I, 5/6 with II and 7/7 for III (I vs III, p less than 0.01). The pericardium is a suitable organ for procurement of endothelial cells. Though reducing yield, filtration and Percoll gradient separation allows for isolation of a relatively pure culture of endothelial cells.

Segments of an experimental polytetrafluoroethylene graft (9 cm long, 6 mm I.D.) of high porosity were implanted in 25 dogs as aortic interposition grafts. Nine grafts were seeded with a mean of 7 x 10(5) viable endothelial cells (ECs) derived from the jugular vein (group A) and eight were seeded with a mean of 7 x 10(5) viable ECs derived from the microvessels of the omentum (group B). Eight grafts were not seeded and they served as controls (group C). Animals were put to death 5 weeks after graft implantation. The thrombus-free area was measured at 81% +/- 10% in group A, 65% +/- 22% in group B, and 25% +/- 13% in group C (p less than 0.05, group A vs group B; p less than 0.05, group B vs group C). The thickness of the subendothelial layer was 151 +/- 60 microns in group A, 280 +/- 60 microns in group B, and 100 +/- 75 microns in group C (p less than 0.001, group B vs groups A and C). The production of 6-keto-PGF1 alpha in the presence of sodium arachidonate was higher in seeded grafts (p less than 0.05). Omentally derived microvessel ECs can be seeded in vascular grafts; refinements in the technique of EC procurement are required to minimize contamination and to obtain ECs with more effective biologic activity.