Napsin A is an aspartic proteinase expressed in some types of carcinomas, such as lung adenocarcinomas and renal cell carcinomas but rarely in squamous cell carcinomas. No specific studies have been carried out focusing on napsin A antibody expression in oral squamous cell carcinomas (OSCC). The aim of this study was to investigate the reactivity of this antibody in primary OSCC. This retrospective study included 70 OSCC cases of which 31 (44.3%) presented metastasis involvement. Patient data, including age, gender, tumor location, histological grade, regional and distant metastasis, were collected. OSCC edge epithelium with intraepithelial neoplasia and healthy oral mucosa (n = 10) were included in the analysis. Sections of lung adenocarcinomas (n = 2) were used as the positive control and an immunohistochemical assay for napsin A was performed on all cases. Napsin A expression was negative in all 70 cases of OSCC, as well as in the intraepithelial neoplasia adjacent to the carcinoma area and in healthy oral mucosa epithelium. Metastatic neck lymph nodes and distant organs were also negative for napsin A. This study shows that napsin A is consistently not expressed in oral squamous cell carcinoma, or in metastatic sites of primary OSCC, intraepithelial neoplasia, and healthy oral mucosa.
Big hospitals and biology museums often have a sizable collection of valuable archived anatomical pathology specimens, collected over a long period of time. Traditionally, these specimens are suspended by thread tied to a frame of glass rods in a rectangular glass jar. While restoring with preserving solution, specimens often fell from sewn thread or strings. We developed an easy method of remounting such specimens on Perspex sheets with cyanoacrylate adhesive. This technique was tested on five archived specimens and five recent well-fixed specimens, including brain. Specimens could be easily oriented, remounted and remained well adhered to the Perspex sheet. Gross pathologic characteristics could be well illustrated from all sides in the remounted specimen. Cyanoacrylate adhesive technique was useful in permanent preservation of old delicate anatomical pathology specimens, which could not be tied to glass rods again and had fallen out of position in mounting jars. This technique can also be applied for well-fixed recent specimens. It is easy, cost effective, serves as an educational tool and can be applied to all types of specimens.
The neural crest cell-derived enteric nervous system (ENS) is the intrinsic innervation of the gastrointestinal tract (GIT) which consists of neurons and enteric glia cells in the myenteric ganglia and forming plexus. The ENS consists mainly of submucosal and myenteric plexuses. It has various functions on the GIT, which include control of local blood flow, motility, mucosal transport, secretions, immune modulation as well as endocrine functions and coordinated contractile activity of smooth muscle. The knowledge on the development of the innervations at different segments of the gut in humans from 11 to 26 weeks of gestation (WG) may help in understanding the pathophysiology of various congenital diseases affecting the ENS. The aim of this study is to determine the morphology of the myenteric plexus in the esophagus, ascending colon and sigmoid colon at various weeks of gestation. Tissue samples from 10 naturally terminated fetuses aged 11-26 WG were processed for hematoxylin and eosin staining and immunohistochemistry assay. The neurons, enteric glia, the smooth muscle were visualized using PGP9.5, Vimentin and S-100 antibodies. The number of neurons and enteric glial cells appeared lowest in the esophagus than the ascending and sigmoid colon. The myenteric ganglion was closely apposed to each other, forming a continuous arch along the entire circumference of gut sections of ascending and sigmoid colon but the myenteric ganglia in the esophagus was thinly populated and widely spread in the fetus at 13 WG. As the fetal gastrointestinal tract grew in diameter and length, the myenteric ganglia became discernible.
Madhuca longifolia, a tropical tree used as medicine and food, is known to have a beneficial effect against stomach gastric toxicity. Madhuca longifolia is used in treating cough, skin disease and nerve disorders. Diclofenac, a non-steroidal anti-inflammatory drug (NSAID), with overdosage and prolonged use, is known to cause gastric toxicity. Silymarin (SLY), a polyphenolic antioxidant flavonoid, is a derivative of Silybum marianum extracted from milk thistle seeds and fruits, has been widely used in the treatment of gastric ulcer. SLY was used as the standard drug to compare the effects with the Madhuca longifolia aqueous leaf extract treatment. The aim of the current study is to understand the effect of Madhuca longifolia aq. leaf extract on rat stomach and intestine against diclofenac-administered toxicity. Rats (n = 30) were divided into Group I normal control, Group II treated with diclofenac, Group III treated with diclofenac and Madhuca longifolia leaf extract, Group IV treated with diclofenac and silymarin, and Group V was treated with Madhuca longifolia leaf extract alone. After the study duration, rats were euthanized and tissue samples were analyzed for antioxidant, cytokine, protein expression levels and histopathological changes. Diclofenac treated rats had significant (p < 0.05) changes in levels of antioxidants, cytokines, protein expression and pathological changes as compared to rats treated with Madhuca longifolia. This study demonstrated that Madhuca longifolia leaf extract had gastroprotective activity in rats treated with diclofenac.
Lung cancer is the leading cancer according to the World Health Organization (WHO), resulting in highest death rate worldwide due to the high level of metastasis. Hence, the drugs that protect from metastasis either as an adjuvant or a primary therapeutic agent may help to reduce the death rate. In this study, All Trans Retinoic Acid (ATRA) was tested for its action against metastatic lodging of B16F10 melanoma cells in the lung and liver of the C57BL/6 mouse model. Serum, lung and liver were evaluated biochemically for the cancer associated changes. Metastatic cancer development was confirmed by tumor nodule formation and histopathological analysis. RAR-β protein expression was analyzed by immunohistochemistry and histopathology. ATRA treated mice showed a percentage of inhibition on metastatic tumor growth in lung and liver and a corresponding protection against pathological changes in these organs. Cholesterol and γ-Glutamyl Transferase (GGT) levels found in cancer induced mice were reduced in the ATRA treated group. As compared to the normal group, lung tissue from cell line induced cancer control group had less RAR-β protein expression while the ATRA treated group showed enhanced RAR-β protein expression. This indicates that the anti-metastasis effects of ATRA might have shown the induction of RAR-β expression and subsequent molecular signaling pathways to regulate the homeostasis of biochemical changes. This study demonstrated the capability of ATRA to prevent the establishment of metastasis by the melanoma cell line into the lung and liver of experimental mice.
Over several decades, there is a growing evidence, which has shown that prenatal stress (PS) contributes to depression in offspring. Grape seed proanthocyanidins (GSPs), which contain dimers, trimers, oligomers of catechin and epicatechin, are known to possess antidepressant effects. The present study aimed to investigate the mechanism of antidepressant effects of GSPs on female juvenile prenatally stressed offspring rats. The results showed that the female juvenile offspring rats exposed to PS exhibited depression-like behavior manifested as longer immobility time and lesser consumption of sucrose solution. Prenatal stress reduced the number of hippocampal neurons and increased the level of the reactive oxygen species (ROS) in the hippocampus of the female juvenile offspring rats. Furthermore, the expression of PYD domains-containing protein 3 (NLRP3) and its downstream cytokines, Caspase-1, and interleukin-1β (IL-1β), were increased in the hippocampus of the female juvenile offspring rats exposed to PS. Administration of GSPs not only improved depression-like behavior and enhanced the number of hippocampal neurons, but also abated excessive ROS generation and inhibited the activation of the NLRP3-Caspase-1 signaling pathway. Taken together, GSPs counteract PS-induced hippocampal neuron loss and depression-like behavior by alleviating oxidative stress and NLRP3 activation. The present study provides a new insight for GSPs as an effective therapeutic agent for adolescent depression.