Medical Molecular Morphology最新文献

We attempted to explore the possible involvement of the in situ availability of mineralocorticoids and mineralocorticoid receptor (MR) in the pathogenesis of mammary ductal carcinoma. We also explored their individual profiles among different subtypes of invasive ductal carcinomas of no special type (IDC-NST) by evaluating the status of MR, Glucocorticoid receptor (GR), and 11β hydroxysteroid dehydrogenase (HSD) 1/2 at each stage of the putative cascade of the mammary ductal proliferative disorders. In this study, IDC-NST, ductal carcinoma in situ (DCIS), atypical ductal hyperplasia (ADH), and non-pathological breast tissues were all evaluated by immunohistochemistry. MR was significantly lower in ADH than in DCIS or IDC-NST. 11βHSD2 was significantly lower in ADH than normal breast tissue and 11βHSD1 was significantly higher in DCIS than normal, ADH, or IDC-NST. MR in progesterone receptor (PR)-positive IDC-NST cases tended to be associated with the Ki-67 labeling index. Results of the present study demonstrated that the status of MR and GR in conjunction with the 11βHSDs was correlated with the development of low-grade proliferative disorders in mammary glands. In addition, the potential crosstalk between MR and PR could also influence cell proliferation of breast carcinoma cells but further investigations are required for clarification.

Both fascin and fibronectin are known to play important roles in cell adhesion and migration. They are noted as tumor markers or inhibiting target for tumor treatment. In this study, embryonic rat livers were obtained to examine the expression of fascin and fibronectin during liver development. Then, the effect of fibronectin on fascin expression was investigated. At embryonic day (ED) 10.5, when the foregut endoderm began to form the liver bud and spread into the septum transversum, fibrous extracellular matrix was observed between the space where the liver bud and the septum transversum merged. At ED11.5, fibronectin was observed surrounding the cluster of fascin-positive hepatoblasts. At ED13.5, hematopoietic cells emerged and both fibronectin and fascin expression started to decline. Fascin and fibronectin appeared temporarily and disappeared by ED 14.5. Their expression was chronologically synchronized. Subsequently, the effect of fibronectin on fascin was examined by cultivation of hepatoblasts that were isolated from the ED13.5 rat liver. As a result, with fibronectin, fascin was positive in most hepatoblasts, although, without fibronectin, fascin expression was remarkably declined. Presently, there are few studies about the relationship between fascin and fibronectin. Our findings suggest that fibronectin could regulate fascin expression in rat hepatoblasts.

Supercooling preservation below 0 °C allows the storage of the transplantable sources in an unfrozen state. This can improve the safety and efficacy of storage by improving the inhibition of metabolism and organ preservation in comparison with conventional preservation at 4 °C. We have developed a supercooling technique using a voltage-applied apparatus without perfusion. We examined the preservation effects of our supercooling preservation technique in a rat model of artery transplantation. Our technique produces a supercooled state at - 2 °C with application of 1000 V. The viability of tissue cells from rat arteries was found to be higher with storage using the proposed method than that under ordinary conditions. Damage to the vascular endothelium of the femoral artery preserved by voltage-applied supercooling at - 2 °C was reduced compared to storage under ordinary conditions. Artery graft revival was successfully achieved with graft patency after supercooling preservation, and 1 week outcomes for post-transplanted grafts, including thrombosis, were better with supercooling preservation than with conventional 4 °C preservation. Supercooling artery preservation at - 2 °C with 1000 V promises to greatly prolong preservation time and improve post-transplant outcomes.

Subarachnoid hemorrhage (SAH) is a complicated and deadly disorder. Dysregulation of miRNAs in SAH has been widely reported. This investigation elucidated the function of miR-23a-3p in the in vivo and in vitro models of SAH. The miR-23a-3p and VCAN levels in SAH rats and sham controls were detected by RT-qPCR. The SAH rats were intracerebrally administrated with miR-23a-3p antagomir. Morphological changes and brain function were assessed. The isolated brain microvascular endothelial cells (BMECs), identified by immunofluorescence staining, were used as the model of SAH in vitro. The viability and apoptosis of BMECs were evaluated using MTT, flow cytometry, and western blotting analyses. Targeted relationship between miR-23a-3p and VCAN was predicted in miRDB and validated by a luciferase reporter assay. We found that the miR-23a-3p level was upregulated in rats after SAH, while VCAN was downregulated. Silencing miR-23a-3p attenuated neurological deficits and neuronal apoptosis in rats after SAH. VCAN was verified to be targeted by miR-23a-3p. Functionally, miR-23a-3p downregulation or VCAN overexpression inhibited BMEC apoptosis and promoted cell activity. Moreover, knockdown of VCAN eliminated the influence of miR-23a-3p inhibition in BMECs. Overall, suppression of miR-23a-3p improves cognitive function after SAH by targeting VCAN.

Purple urine bag syndrome (PUBS) is seen in the prolonged indwelling bladder catheters, and the mechanism of its onset was investigated using low vacuum scanning electron microscopy (LVSEM), which enables us to study the 3D structure of urinary sediments and urine bag walls. The urinary sediment and urine bags of 2 cases of PUBS were observed by LVSEM. The urine was brown turbid urine with a pH of 8.5, and magnesium phosphate stones and granules were observed in the urinary sediment together with Gram-positive and Gram-negative bacilli. Bacteria that moved by Brownian motion were observed with a dark-field microscope. LVSEM showed granular crystals around the bacilli, cocci, or mycelium that adhered to the walls of the bag. Granular crystals were dissolved in chloroform and presumed to be a mixture of the bacterial metabolites indigo blue and indirubin red. LVSEM also detected unusual tubular and honeycomb-like graphene in the urinary sediments, which were derived from the inner layer of the silicon elastomer-coated rubber catheter. LVSEM revealed purple crystals produced by bacteria or fungi attached to the urine bag that caused PUBS.

Endometriosis is a benign tumor that affect 6-10% women of reproductive age. To date, it is suggested that the aberrant microRNA (miRNA) expressions play important roles in the pathogenesis of endometriosis. Reviewing the literature, we found nine overexpressed miRNAs, which were thoroughly investigated in the context of endometriotic tissues and cells. Most of the overexpressed miRNAs induced endometriosis-specific characteristics including inhibition of apoptosis and decidualization, upregulation of fibrogenesis, invasion, migration, cell proliferation, attachment to extracellular matrix, inflammation, and angiogenesis in the endometriotic cells. Then, we found that the downstream target molecules of these miRNAs, such as early growth response protein-1, extracellular signal-regulated kinase, matrix metallopeptidase 1, signal transducer and activator of transcription 3, cyclooxygenase-2, phosphoinositide 3-kinase, AKT, mammalian target of rapamycin, and vascular endothelial growth factor-A are promising for the therapeutic targets of endometriosis. Recent findings suggest that complex molecular mechanisms leading to development and progression of endometriosis by miRNAs may exist in endometriosis. The meticulous balance between tumorigenic miRNAs and tumoristatic miRNAs may destine the natural course and response to the surgical, medical, and hormonal treatments of this disease. Further investigations into endometriosis-associated miRNAs may elucidate the pathogenesis of endometriosis and help to develop novel therapeutics.