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For centuries, histology has maintained its remarkable place in the medical curriculum. However, its teaching has been influenced by the new technological advancement that has reshaped medicine teaching into a more modern student-friendly form. Since its inception in the 18th century, the discipline of histology has progressed hand in hand with the advancements in microscopy and microscopic technologies, including immunohistochemistry.In the traditional curriculum of USA medical schools, especially after the first Flexner's report of 1910, histology was considered as very essential topic for a physician studying the "Art and Science" of medicine. In this era, the teaching relied more on the light microscope and to some extent on the electron microscope. However, the field nowadays, after the second Flexner's report, which stressed the importance of integrating clinical topics in the curriculum, is shifting towards the use of more electronic resources for teaching. Such new resources rely on information technology and electronic imaging modalities which are considered to be more student-friendly, time efficient, consistent in conveying the images, promote self-learning and are less costly. In fact, in the last 25 years, most universities started relying on virtual microscopy with limited use of the light microscopy by the students. Such an approach facilitated curricular integration of histology into histopathology and provided the opportunity to promote self-learning and clinical relevance. In the era of competency-based curriculum, histology remains an essential and indispensable basic science in the integrated modules.

The myofibroblast, a major component of granulation tissue, is a key cell during wound healing, tissue repair and connective tissue remodelling. Persistence of myofibroblasts within a fibrotic lesion leads to excessive scarring impairing function and aesthetics. Various wound-healing cytokines can be modulated by topical application of active agents to promote optimal wound healing and improve scar quality. Thus, the myofibroblast may represent an important target for wound-healing modulation to improve the evolution of conditions such as hypertrophic scars. The purpose of this work is to study the modulation of myofibroblasts and integrin alphavbeta3 in a full thickness wound performed on rabbits treated with different topical agents using: (1) saline, (2) Tegaderm occlusive dressing (3) silver sulfadiazine and (4) moist exposed burn ointment (MEBO). The reepithelialisation was 4 days faster in the MEBO group compared with the other therapies with less oedema formation, delayed contraction, less inflammatory cells and the lowest transepidermal water loss (TEWL) resulting in a soft scar. Although alpha-smooth muscle actin (alpha-SMA) was the highest around day 12 in the MEBO group, wound contraction and myofibroblast's activity were the least for the same period probably because of a downregulation of the integrin alphavbeta3. It seems that the effect of MEBO could be more pronounced on force transmission rather then on force generation. Greater insight into the pathology of scars may translate into non surgical treatments in the future and further work in myofibroblast biology will eventually result in efficient pharmacological tools, improving the evolution of healing and scar formation.

This study aims to describe the morphological alterations in the small and large intestines as well as the expression of some enterocyte enzymes and carriers in a rat model of iodoacetamide-induced colitis. Biopsies from the large and small intestines were taken at 1, 2, 4, 8, and 16 days postinduction and studied by light microscopy. The expressions of lactase, sucrase, aminopeptidase, and Glut-5 in the jejunum were studied by immunohistochemistry. Gene expressions of enterocyte lactase and sucrase were determined by RT-PCR using specific oligonucleotides. Microscopic examination of the large intestines revealed manifestations concordant with inflammation. Such alterations peaked at 2 days, were maintained to a lesser extent for 4 days, regressed by 8 days, and healed by 16 days. In the jejunum, the expression of lactase, sucrase, and aminopeptidase decreased 2 days after colitis induction, and recovered 2 days later. Similarly, Glut-5 expression decreased transiently with partial recovery by day 8. Compared with sham, gene expression of jejunal brush border enzymes sucrase and lactase showed a 4-fold increase in lactase and a 9-fold increase in sucrase after 4 days. We conclude that colitis can induce significant functional abnormalities in distant noninflamed small bowel regions.

The co-occurrence of colorectal cancer (CRC) and diabetes mellitus along with inflammation and dismicrobism has been frequently reported. Several studies shed light on the antioncogenic potential of metformin on colorectal carcinogenesis. This study aimed to demonstrate that metformin in association with probiotics acts in a synergic effect in breaking the crosstalk, thus inhibiting CRC progression, improving diabetes, and reducing inflammation. Ninety-six male Balb/c mice, 6–8 weeks old, were divided into 16 control and experimental groups to assess the effect of the different treatments and combinations at the clinical, histological, and molecular levels. Metformin and probiotics showed beneficial outcomes on CRC and diabetes, alone and most importantly in combination. Their effects were exerted by inhibiting the inflammatory process whereby a downregulation of IL-6 and TNF-α as well as oxidative stress were depicted. The characterization of the effects of probiotics and metformin on CRC and diabetes sheds light on the role of inflammation and microbiota in this crosstalk. Deciphering the downstream signaling pathways elicited by these compounds will help in developing new effective targeted treatment modalities.

Objectives:Arterial stiffness is becoming a major global condition associated with an increased risk of cardiovascular problems and death. Several markers have been linked to arterial stiffness.Methods:To determine and evaluate these relations, anthropometric parameters (weight, height, and pulse rate), biochemical profile, and central and peripheral indices of arterial function were measured in 114 Lebanese subjects with Grade I essential hypertension.Results:Age was associated with a higher pulse wave velocity (p = .001), central systolic blood pressure (p = .013), central pulse pressure (p = .028), central augmentation index (p ≤ .0001) with a lower heart rate (p = .08), and glomerular filtration rate (p = .019). Pulse wave velocity was found to be higher in older subjects (>65 years) and correlated with higher body mass index (r = .85) independent of age. Aging also correlated with higher plasma glucose and alterations in calcium–phosphorus metabolism.Conclusion:Aging is associated with increased arterial stiffness which is reflected by an increase in the pulse wave velocity, augmentation index, central pulse pressure, and central systolic blood pressure with a reduction in heart rate. Also, a higher body mass index and a lower estimated glomerular filtration rate (< 60 mL/min/1.73 m2) are associated with increased arterial stiffness while calcium and phosphorus metabolism may play a role by promoting vascular calcification.

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This study assessed the effect of catechin in modulating the inflammation of colitis. Thirty rats were randomized into three groups: Group I: chemically induced with colitis and received no treatment, Group II: chemically induced with colitis and received daily injection of EGCG, Group III: control group provided with water only. In groups I and II, colitis was induced by TNBS solution. Rats were sacrificed on days 3, 10 and 17 and biopsies of distal colons were assessed by histology and molecular techniques for ROS and changes in cytokines like IL-6 and IL1-β. Colitis induced by TNBS and non-treated with EGCG group, showed high inflammatory scores resulting in colonic mucosa and submucosa damage, necrosis, absence of goblet cells, infiltration of inflammatory cells, crypt abscesses and granulomas. Infiltration of inflammatory cells and tissue damage peaked at day 17 after the induction. At day 3 and day 10, the treated rats with EGCG showed amelioration in the severity of inflammation, but at day 17, the state of the colonic crypts and goblet cells was close to normal. The number of mast cells in the colon of treated rats decreased by more than 30% at day 17 compared to the non- treated rats. In addition, the expression of ROS decreased significantly. IL-1B and IL-6 expressions decrease with time by 50% in the treated group. Our data confirmed the anti-inflammatory effect of EGCG in TNBS-induced colitis and provided a clue to a potential therapeutic agent.