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Lung Cancer (a) Diagnosis and Causes, Smoking Habits, etc.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
Primary pulmonary adenocarcinomas are of several types (see above), and should be differentiated (if possible) from metastases (e.g. from pancreas, alimentary tract, ovary, etc.). Acinar tumours are probably derived from the mucus-secreting cells in the bronchial mucosa of small peripheral bronchi, and on microscopy acini, ducts and tubules may be found. Mucus formation is common, particularly with some bronchiolo-alveolar tumours, and this may lead to severe distress in about 5% of cases. Mixed adeno-squamous types are not uncommon. Some adenocarcinomas arise in pulmonary scars. Bronchiolo-alveolar tumours - ps. 5.1 - 5.4 grow along existing alveolar walls before spreading out into the bronchioles, bronchi and surrounding tissues, then via the airways and lymphatics.
The salivary glands
Published in Neeraj Sethi, R. James A. England, Neil de Zoysa, Head, Neck and Thyroid Surgery, 2020
The basic unit of a salivary gland consists of an acinus, a secretory duct and a collecting duct. The acinus has a central lumen surrounded by pyramidal-shaped cells and myoepithelial cells. It produces the primary secretion. Acini are classified as serous (numerous cytoplasmic granules), mucous (clear cytoplasm) or mixed.The secretory ducts are composed of intercalated and striated ducts, which are intralobular. They make saliva hypotonic by taking in Na+, releasing K+ and excreting HCO3−.The collecting ducts are composed of two cell layers – the inner flat cells and the outer columnar cells. When the myoepithelial cells contract, preformed secretions are expelled through the duct [3].
ExperimentaL Oral Medicine
Published in Samuel Dreizen, Barnet M. Levy, Handbook of Experimental Stomatology, 2020
Samuel Dreizen, Barnet M. Levy
Leake et al.78 detailed the ultrastructural changes in the rat parotid gland after ligation of Stensen’s duct. The duct was ligated unilaterally in 18 mature Sprague-Dawley rats, and the parotid gland was examined by electron microscopy at intervals up to 90 days. The course ran from swelling and engorgement lasting 4 to 6 days to progressive atrophy. At 3 months, the number of identifiable acini was greatly decreased. Nuclei in the few remaining acinar cells were prominent because of the lack of secretory granules in the cytoplasm. Endoplasmic reticulum was severely disorganized and sometimes absent. Golgi apparatus was markedly decreased. Microvilli were truncated with blunt ends. Cell borders remained distinct with well-demarcated desmosomes. There was an increase in collagen and infiltration of some inflammatory cells in the areas formerly occupied by the acini.
Vitamin E protects against the modulation of TNF-α-AMPK axis and inhibits pancreas injury in a rat model of L-arginine-induced acute necrotising pancreatitis
Published in Archives of Physiology and Biochemistry, 2023
Fahaid Al-Hashem, Mohamed Abd Ellatif, Asmaa M. ShamsEldeen, Samaa S. Kamar, Bahjat Al-Ani, Mohamed A. Haidara
In view of the results described above that showed substantial protection by vitamin E to L-arg-modulated biomarkers of inflammation, pancreatic tissue necrosis, AMPK, and leukocyte infiltration, we investigated whether vitamin E can also protect pancreatic tissue against injury induced by L-arg in a rat model of acute pancreatitis using morphological and histological investigations. Thus, explanted pancreases from all animal groups were examined and tissue samples were prepared for basic histology staining. Compared to normal macroscopic images in the control groups of rats (Figure 5(A), I and data not shown), L-arg induced swelling with patchy areas of haemorrhage (Figure 5(A), II). Vitamin E treatment (Figure 5(A), III) substantially but not completely preserved the pancreas morphological structure. Representative H&E images of the pancreatic tissue obtained from the control groups of rats (Figure 5(B), I and data not shown) show the regular architecture of pancreatic tissue as demonstrated by multiple lobules separated by thin connective tissue (CT) septa, with each lobule forming multiple acini lined with pyramidal cells. These cells show basal rounded pale nuclei, basal basophilic cytoplasm, and apical acidophilic granules. H&E image represents pancreatic sections of the model group (L-arg) of rats (Figure 5(B), II) which shows disorganised lobular architecture with inflammatory infiltration within the CT septa. The acini appear with multiple cytoplasmic vacuolations and pyknotic nuclei. In addition, the presence of congested blood vessels and extra-vasated blood in between the acini are revealed.
The efficacy of Origanum majorana nanocubosomal systems in ameliorating submandibular salivary gland alterations in streptozotocin-induced diabetic rats
Published in Drug Delivery, 2022
Dina B. E. Farag, Carol Yousry, Abdulaziz Mohsen Al-Mahallawi, Hesham I. El-Askary, Meselhy R. Meselhy, Nermeen AbuBakr
H&E-stained submandibular salivary gland sections of the diabetic untreated rats (group I) revealed severely distorted architecture. The glandular acini demonstrated loss of regular acinar configuration. Acinar blurred boundaries, loss of acinar cell septum, as well as massive cytoplasmic vacuolization were clearly demonstrated in most of the acini. Degenerative areas were evident in the granular convoluted tubules (GCTs) with obvious loss in cytoplasmic content as well as ductal cell vacuolization. The striated ducts showed indistinctly cellular basal boundaries with loss of basal striations (Figure 4(A)). Thinning and deformation of the epithelial lining of the excretory duct with loss of pseudo stratification were detected. The cell nuclei were flattened and apically displaced. Dissociated periductal connective tissue, as well as dilated congested ruptured blood vessel, was also observed (Figure 5(A)).
Assessment of small intestinal bacterial overgrowth in chronic pancreatitis patients using jejunal aspirate culture and glucose hydrogen breath test
Published in Scandinavian Journal of Gastroenterology, 2021
Rajesh Sanjeevi, Kapil Dev Jamwal, Sudipta Dhar Chowdhury, Balamurugan Ramadass, R. Gayathri, Amit Kumar Dutta, Anjilivelil Joseph Joseph, Balakrishnan S. Ramakrishna, Ashok Chacko
Chronic pancreatitis is a syndrome of chronic progressive pancreatic inflammation and scarring, leading to irreversible damage of the pancreas with resultant loss of exocrine and endocrine function [1]. Pancreatic exocrine insufficiency (PEI) is an under-recognized problem amongst patients with chronic pancreatitis [2]. Destruction of pancreatic acini reduces pancreatic enzyme secretions resulting in PEI. Though lipid digestion is predominantly affected, PEI can also lead to carbohydrate and protein maldigestion [3]. PEI can lead to bloating, steatorrhoea or diarrhea and significantly impair the quality of life [4]. Changes in pancreatic exocrine function have been shown to produce changes in microbial diversity within the gastrointestinal tract [5]. One such pathological form of microbial dysbiosis that occurs in chronic pancreatitis is small intestinal bacterial overgrowth (SIBO). SIBO has been defined as a clinical syndrome caused by the presence of an excess amount of bacteria in the small bowel [6]. Symptoms of SIBO can mimic symptoms of PEI. Factors that predispose chronic pancreatitis patients to SIBO include decreased pancreatic proteolytic enzymes, use of narcotics, ethanol use, use of proton pump inhibitors (PPIs) and diabetic neuropathy [7–10].