Medical Molecular Morphology最新文献

Gastrointestinal tumors significantly contribute to cancer-related mortality worldwide. Early detection coupled with effective treatment significantly improves overall survival. Immunoglobulin G (IgG) N-glycosylation, a crucial post-translational modification, undergoes alterations in glycan structures. IgG N-glycosylation is associated with numerous physiological and pathological processes in the human body. Aberrant changes of IgG N-glycosylation play a key role in cancers given the involvement of glycans in cancer progression and immune modulation. These changes affect the binding of the Fc region of IgG to its receptor, in turn, affect the corresponding downstream effects, which are crucial in cancer immuno-surveillance and immune escape. This review aims to explore the latest advancements in understanding IgG N-glycosylation in gastrointestinal cancers, emphasizing its potential as a diagnostic biomarker and therapeutic target. The application of IgG N-glycosylation in clinical oncology could enhance early detection, improve therapeutic efficacy, and enable better monitoring of disease progression and recurrence. Furthermore, we summarized the research progression to provide novel insights into the potential regulatory mechanism of IgG N-glycosylation in gastrointestinal tumors. In all, IgG N-glycosylation holds significant promise for advancing cancer diagnosis and treatment. Further studies are required to fully elucidate its mechanisms and optimize its use in clinical practice.

Mucoepidermoid carcinoma in the lung is uncommon, while the occurrence of a collision tumor consisting of primary mucoepidermoid carcinoma (MEC) and typical adenocarcinoma is extremely rare. We report a case of a 70-year-old female with the presence of a nodule in her right lung. The pathological examination revealed a primary collision tumor consisting of invasive adenocarcinoma and mucoepidermoid carcinoma. Manual microdissection was performed to selectively isolate the MEC and adenocarcinoma components, followed by exome sequencing which unveiled identical mutations in both components, suggesting their monoclonal origins with divergent differentiation. Clinical awareness and recognition of such collision tumors are crucial, as they will determine appropriate treatment strategies based on the individual biological aggressiveness of each tumor component.

The placenta is the most critical organ during pregnancy and its developmental status directly impacts fetal health. Placental dysfunction is associated with various pregnancy complications, including preterm birth, fetal growth restriction, and premature rupture of membranes (PROM). This study aimed to elucidate the expression changes of Bax and Bcl-2 and their association with pregnancy-related complications, providing new insights into placental dysfunction during pregnancy and offering a theoretical foundation for clinical diagnosis and prevention. The placental samples from 118 late pregnant women were retrospectively analyzed. They were assigned into pre-term, term, post-term, PROM, and non-PROM groups based on gestational age and the occurrence of PROM. Immunohistochemistry (IHC) staining was performed to gauge the Bax and Bcl-2 expressions in placenta. Receiver operating characteristic (ROC) curve was subsequently conducted to assess their associated with efficacy for PROM. The weight and volume of placentas in the pre-term group were sharply smaller to those in the term and post-term groups, with no apparent fibrosis or calcification observed. The term and post-term groups exhibited marked elevated Bax expression in the parturient group in contrast to the non-parturient group (P < 0.05), while there existed no substantial significance in Bcl-2 expression. The area under the curve (AUC) for Bax and Bcl-2 was 0.975 and 0.596, respectively, with a combined associated with value of 0.978, higher to single predictions. Bax and Bcl-2 expressions in late pregnancy placentas were associated with the onset of parturient status and PROM and their combined prediction exhibited accurate PROM predicted. These findings offered a new perspective for understanding the physiological and pathological changes of the placenta during pregnancy.

Background: With the extensive application of flap surgery in clinical practice, it has been a matter of great concern to improve the survival rate of flap surgery for a long time. This study compared and explored the effect of the three generations of platelet concentrates (PCs), including platelet-rich plasma (PRP), platelet-rich fibrin (PRF), and concentrated growth factor (CGF), on flap survival.

Methods: After PRP, PRF, and CGF gels were observed by scanning electron microscope (SEM), their vascularizing effect were assessed by infrared thermal imager, flap survival experiment, arterial perfusion angiography, and immunohistochemical staining in a rat dorsal cross-region perforator flap model.

Results: The fibrin of PRP gel showed irregular clumps and loose structure, while that of PRF and CGF gels formed 3D network structure with orderly arrangement and compact structure. In animal models, the use of all the three PCs can increase the number of vessels and the amount of blood perfusion in choke zones (all P < 0.05), thus improving the flap survival rate. Moreover, the effects of CGF and PRF were obviously better than those of PRP (all P < 0.05), but there was no significant difference between CGF and PRF (P > 0.05).

Conclusions: PRP, PRF, and CGF all have a good effect on promoting vascularization, and can significantly improve the survival rate of dorsal cross-region perforator flap in rat model. Besides, PRF and CGF have greater potential in promoting vascularization than PRP.

Placenta accreta spectrum (PAS) is a serious disease leading to complications and maternal death. The objective of the study was to characterize the placental villi and blood vessels of PAS villi histopathologically. We investigated 10 cases of PAS (five cases of placenta increta, two cases of placenta accreta, and three cases of placenta percreta) histologically. Immunohistochemical staining using anti-CD68 or anti-CD163 antibodies was performed to detect and count Hofbauer cells. Immunohistochemical staining with an anti-CD34 antibody was used to detect vascular endothelial cells, and the number and area of vessels were analyzed. The numbers of CD68-positive or CD163-positive Hofbauer cells were larger in PAS cases compared with control cases. The vascular area in villi was smaller in PAS cases compared with control cases. The number of blood vessels in villi was slightly higher in PAS cases than in control cases. The numbers of Hofbauer cells and vessels in villi were larger in PAS cases compared with control cases, whereas the area of vessels in villi was smaller in PAS cases compared with control cases. Although their biological meaning is elusive, these findings provide novel insights into the pathogenesis of PAS, particularly regarding the role of Hofbauer cells in immune-suppressive role and angiogenesis and the alterations in vascular structure and hemodynamics in the chorionic villi.

Dry eye is a multifactorial ocular surface disease that may be accompanied by visual impairment and ocular surface damage. Thrombospondin 1 (THBS1) was found to be highly expressed in corneal epithelial cells of dry eye mouse models. Our research aimed at exploring the role and regulatory mechanism of THBS1 in dry eye mouse models. Both eyes of mice with benzalkonium chloride (BAC)-induced dry eye were subconjunctivally injected with the recombinant adeno-associated virus (AAV) vector containing the THBS1 silencing plasmid. Under a slit lamp biomicroscope, the conjunctival irritation including edema, hyperemia, and secretion was scored. Fluorescein staining was performed to evaluate corneal epithelial damage. The conjunctiva tissues were obtained for ELISA, RT-qPCR, histological staining, and western blotting. Dry eye model mice exhibited severe ocular surface damage, reduced tear secretion, conjunctival goblet cell loss, increased conjunctival inflammation, elevated THBS1 expression, and the TGF-β/NLRP3 inflammasome pathway activation. THBS1 silencing ameliorated ocular surface damage, increased tear secretion, attenuated conjunctival goblet cell loss, mitigated conjunctival inflammation, and repressed the TGF-β/NLRP3 inflammasome pathway activation in dry eye mice. THBS1 silencing protects mice against dry eye by inhibiting TGF-β/NLRP3 inflammasome-mediated inflammatory response.

We report a rare case of thymoma with extensive clear cell components, and discuss the histogenesis of clear cell transformation. Although thymic clear cell carcinoma is classified as a subtype of thymic carcinoma, thymoma with extensive clear cell components has not been recognized as a subtype in the World Health Organization classification (2021). Therefore, such thymomas may be erroneously misdiagnosed as clear cell carcinoma. Thymic clear cell carcinomas are positive for glycogen, with a high Ki67 index, whereas the clear cell component of the present tumor was negative, with a low index; this difference may help to distinguish thymomas with extensive clear cell components from thymic clear cell carcinomas. In this tumor, spindle cells predominantly proliferated in the center, whereas clear cells were densely distributed in the periphery. Hence, the initial tumor likely consisted of spindle cells, some of which transformed into clear cells as the tumor grew larger. In addition, nuclei of the clear cells were occasionally positive for autophagy-related 4 cysteine peptidase. Electron microscopically, clear cells with eccentrically located nuclei and cytoplasm contained large vacuoles, in which irregularly shaped membranous structures were observed. The histology, immunohistochemistry, and ultrastructure suggest that clear cell transformation represents a type of cellular degeneration.

Primary squamous cell carcinoma (SCC) of the renal parenchyma is exceedingly rare, with only seven cases reported to date. We report a 72-year-old woman with recurrent cystitis, gross hematuria, and a right renal mass. Imaging studies revealed a necrotic lesion in the renal parenchyma, initially suggestive of an abscess. Despite percutaneous drainage and antibiotic therapy, there was no clinical improvement. Trans-urinary tract fine-needle aspiration (FNA) provided preoperative cytologic evidence of malignancy with features consistent with SCC, and histopathologic examination of the nephrectomy specimen, supported by immunohistochemistry, confirmed primary renal parenchymal SCC. The patient subsequently underwent radical nephrectomy, and histopathological examination confirmed a primary SCC of the renal parenchyma without renal pelvic involvement. Although surgical treatment was performed promptly, metastatic spread to lymph nodes, vertebrae, and lungs was detected within months, and the patient died 18 months postoperatively. This case highlights the importance of considering SCC in the differential diagnosis of abscess-like renal lesions, particularly when they fail to respond to antibiotics. In selected patients, trans-urinary tract FNA offers a rapid, minimally invasive means to obtain cytologic material, which can prevent delays and facilitate timely management, potentially improving outcomes in similarly challenging cases. Additional studies will clarify diagnostic and therapeutic strategies.

Ovarian cancer (OvCa) is a leading cause of gynecological cancer-related mortality, primarily due to peritoneal dissemination, which facilitates metastasis in the abdominal cavity. This study explored the potential of vitamin D and its synthetic derivatives in mitigating peritoneal dissemination by modulating the behavior of mesothelial cells (MCs). Vitamin D, through its receptor (VDR), is known to influence cancer progression, and our findings demonstrate that vitamin D derivatives can inhibit mesenchymal transition of MCs induced by TGF-β1, a key driver of peritoneal dissemination. This study used patient-derived primary MCs and in vivo mouse model to assess the effects of vitamin D derivatives on cell morphology, gene expression, and OvCa cell adhesion. Two vitamin D derivatives, VDR agonist, showed significant efficacy in maintaining epithelial-like MC morphology, reducing TGF-β1-induced changes, and inhibiting OvCa cell adhesion to the peritoneum, similar to calcitriol. Conversely, the VDR antagonist derivative induced MC apoptosis, highlighting the essential role of vitamin D in MC survival. These findings suggest that vitamin D derivatives could serve as promising therapeutic agents for OvCa by preserving peritoneal homeostasis and preventing metastasis. Further research is required to explore a broader range of derivatives and their underlying molecular mechanisms.

The palmar plate is a crucial structural part of hand, associated with metacarpophalangeal and interphalangeal joints. Pediatric disorders involving the palmar plate of thumb metacarpophalangeal joint include trigger thumb, hyperextension, instability, and dislocation. While anatomical differences exist between children and adults, detailed microstructure evaluations in infants remain unexplored. In this study, we provide a histological and structural assessment of the previously unresolved microstructure of the palmar plate in the thumb metacarpophalangeal joint of infant Japanese macaques (Cercopithecidae, Macaca fuscata), a relevant model for human development. Histological staining (light microscopy) and scanning electron microscopy were employed to visualize the three-dimensional microstructure. The palmar plate of the infant macaque was found to contain (1) elastic fibers, (2) hyaline cartilage composed of type II collagen, and (3) type I collagen fibers arranged in distinct patterns. The cartilaginous region exhibited a reticulate fiber arrangement on its periphery, while the membranous region displayed dense and complex fibers on the proximal phalanx side and parallel on the metacarpal side, respectively. This is the first comprehensive three-dimensional investigation of the infant's thumb's palmar microanatomy, providing a foundation for understanding its development and implications for pediatric disorders.