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Since its outbreak in early 2020, the COVID-19 pandemic has diverted resources from non-urgent and elective procedures, leading to diagnosis and treatment delays, with an increased number of neoplasms at advanced stages worldwide. The aims of this study were to quantify the reduction in surgical activity for indeterminate thyroid nodules during the COVID-19 pandemic; and to evaluate whether delays in surgery led to an increased occurrence of aggressive tumours.

Immunological and biochemical reactions associated with inflammation are elicited in response to a physical or immunological challenge. Early in inflammation there is mobilization and infiltration of neutrophils, mast cells and macrophages to the site of inflammation. These cells release pro-inflammatory compounds icluding cytokines, vasoactive peptides (eg., histamine), and eicosanoids. The release of prostaglandin D2 (PGD2) and tryptase induced by anti-IgE, A23187 and compound 48/80 were studied using in vitroa good and valid model of human cord blood-derived mast cells (HCBDMC). Tryptase is a mast cell product and enhances vasopermeability with anticoagulant activities. In this study we measure the release of PGD2 and tryptase on mast cells activate by anti-IgE, calcium ionophore A23187, polybasic compound 48/80 (an agent containing a cationic region adjacent to a hydrophobic moiety, which works by activating G proteins) and IL-18. The generation of PGD2 was measured by radioimmunoassay. Release of PGD2 was detectable (after 12 h) following challenge with anti-IgE, A23187 and compound 48/80. Our data show that mature HCBDMC produce proinflammatory PGD2 following triggering with anti-IgE and with IgE-independent agonists, such as calcium ionophore A23187 and polybasic compound 48/80, while IL-18 was unable to stimulate the release of PGD2 or tryptase on HCBDMC. Although a great deal has been learned about the mediators produced by mast cells, the ultimate biologic function(s) of mast cells remains a mystery.

Atherosclerosis is an inflammatory disease due to a diet high in saturated fat, hypercholesterolemia, obesity, hypoglycemia, etc. mainly mediated by the infiltration of macrophage and T cells into the vascular wall. Once the endothelial is damaged monocytes penetrate the tissue and are transformed in scavenger cells. Upon stimulation of Th1 cells, a group of cytokines is released and contributes to the inflammatory response of atherosclerotic tissue. When macrophages proliferate they amplify inflammatory response through the secretion of growth factors and cytokines such as TNF and IL-1. In addition, chemokines such as RANTES and other C-C chemokines are generated, and matrix metalloprotinease 9 (MMP-9) are produced by activated monocytes. However, the immune system in atherosclerosis still remains unclear. Here, in this study we revisited the inter-relationship between atherosclerosis and inflammation.

Obesity is one of the main rising causes of health problems in modern society and is correlated to type 2 diabetes mellitus, hypertension, heart disease and atherosclerosis. Bacterial products, endogenous substances such as oxidized LDL (ox-LDL) and heat shock proteins mediate activation of Toll-like receptors and reinforce the view that the innate immune system plays a key role in the genesis of atherosclerosis. In addition, natural killer T (NKT) cells respond to lipids presented via CD1d on APCs, and may also be able to affect atherosclerosis. All the main cell types involved in atherosclerosis such as endothelial cells, macrophages, T cells, smooth muscle cells and platelets express proinflammatory cytokines. In addition, CD4 ligation triggers the expression of adhesion molecules, cytokines and matrix metalloprotinease. IL-6 cytokines travels to the liver where it elicits acute phase response resolving in the release of serum amyloid-A C-reactive protein, fibrogen and plasminogen activator inhibitor-1. Therefore increasing body fat mass is associated with high levels of inflammatory cytokines such as IL-1 and TNF. In this study we revisit the interrelationship between fat and inflammation.

Purpose To report pre- and post-operative macular optical coherence tomography (OCT) and immunohistochemical findings in a case of long-lasting silicone oil tamponade followed by silicone oil removal and epimacular membrane peeling.Methods A 69-year-old man with long-standing silicone oil tamponade and an epiretinal membrane at the posterior pole in his right eye (RE) underwent silicone oil/BSS exchange with epiretinal membrane peeling. Preoperatively RE best-corrected visual acuity was 20/200 and macular OCT examination revealed a small increase in foveal thickness (250 μm) with the appearance of a linear hyper-reflective signal at the foveal vitreoretinal interface and a thicker (440 μm) hyperreflective finding causing posterior shadowing at the vitreoretinal interface inferiorly to the fovea. Histopathologic and immunohistochemical study of the specimen including the epiretinal membrane was performed.Results Light microscopy revealed extensive rounded empty spaces interpreted as silicone oil bubbles in the preretinal membrane. Macrophages marker (CD68) positive staining cells were found surrounding the empty spaces within the preretinal membrane and several empty spaces were observed intracellularly within macrophage cytoplasm. Thirty days after surgery best-corrected visual acuity was 20/60 and OCT examination showed an evident decrease in foveal thickness (220 μm) with the disappearance of any hyper-reflective signal at the vitreoretinal interface referable to an epiretinal membrane.Conclusions The immunohistochemical study showed both silicone oil droplets and macrophagic cells embedded in the epiretinal membrane. Postoperative OCT demonstrated retinal recovery after silicone oil removal and epiretinal membrane peeling, thus justifying an unexpected visual acuity recovery despite the very long term tamponade.

Vascular Endothelial Growth Factor, also known as Vascular Permeability Factor, is a multifunctional cytokine hyperexpressed during angiogenesis and in numerous physiological and pathological processes characterised by an increase of vascular permeability. The aim of this study was to evaluate the angiogenetic processes which are accompanied by an expansion of cystic radicular lesions and of keratocysts of the jaw bone. 12 subjects were chosen with an average age of 43 years, of whom 8 were males and 4 females. After an accurate history and physical examination, the patients underwent surgery for removal of the cysts. The samples taken were histologically and immunohistochemical examined. The histological exam confirmed the diagnosis of radicular cysts and keratocysts. The immunohistochemical examinations were positive for VEGF in all the lesions analysed, even though they had different immunostaining. Using a semi-quantitative method, in the radicular cyst samples it was possible to highlight a wider expression of the vascular component, both in the inflamed area and the adjacent stroma. The lesions with keratin content showed newly formed and modest vascularisation both in the area showing slight inflammation, where the cellular component was prevalent, and in the adjacent areas showing no inflammation. Therefore, angiogenesis could take on a primary role in the development of cystic lesions of the jaw. However, the differences of expression of the VEGF protein suggest the need for wider monitoring to better evaluate a possible use of such a protein as a diagnostic marker.

The aims of the present study were: (i) to assess whether H. pyloricould be succesfully detected by PCR from the same biopsy sample used for CPtest; and ii) to evaluate CPtest comparatively to both PCR and histology for detection of H. pyloriinfection in dyspeptic patients. Three antral gastric biopsies were collected from each of 80 consecutive dyspeptic patients undergoing oesophagogastroduodenoscopy. Two biopsies were for histology (gold standard), one for CPtest, scored at 20min, 1h and 24h for the presence of urease activity. Gastric biopsy was then removed from CPtest and used for ureC-targeted PCR. Fifty-five (68.7%) patients were positive for H. pyloriinfection by histology. CPtest yielded an overall diagnostic accuracy of 93.8% (95% CI: 91–96.4%), regardless of observation period. No erroneous categorization of H. pyloristatus occurred using PCR, yielding sensitivity, specificity, positive and negative predictive values, and overall diagnostic accuracy of 100%. Our results suggest that H. pylorican be detected by PCR in gastric biopsies previously taken for CPtest, so reducing the workload of the endoscopist by saving additional biopsies for culture analysis and susceptibility tests.

Histological detection of axillary lymph node metastases is still the most valuable prognostic parameter for breast cancer, but about 30% of node-negative patients relapse within five years, suggesting that current methods are inadequate for identifying metastatic disease. More sensitive, PCR-based methods for the detection of metastatic cells are now available, enabling the amplification of cancer cell-specific mRNA messages by the RT-PCR assay. An ideal tumour marker, consistently expressed in tumour samples and not at all in normal lymph nodes, remains to be identified. The present study first investigated the expression of seven mRNA markers, CEA, CK19, c-Met, mammaglobin, MUC-1, β1→GalNAc-T and p97, selected on the basis of their previously reported specificity for breast cancer cells. Eighteen lymph nodes were examined from patients without tumours. Only mammaglobin mRNA and CEA mRNA were not expressed in normal nodes. All of the other markers showed a band of expression in 17%-55% of cases, indicating that they are not breast cancer-specific. CEA mRNA and mammaglobin mRNA expression could be detected in 15/20 (75%) and 19/20 (95%) primary breast carcinomas, respectively. The expression of mammaglobin mRNA and CEA mRNA was then compared in axillary lymph nodes from 248 consecutive breast cancer patients, 89 with histologically documented lymph node metastasis and 159 without histological evidence of metastatic disease. Ninety-seven per cent of the patients with histologically involved nodes showed expression of mammaglobin mRNA, whereas CEA mRNA was expressed in 79% of these cases. In the group of patients with histologically negative lymph nodes, 46 (29%) and 32 (20%) were found to be positive for mammaglobin and CEA expression, respectively, indicating the presence of metastases not detected by routine histological examination of one lymph node section. These results show that both mammaglobin RT-PCR and CEA RT-PCR are useful tools for the detection of breast cancer metastases in axillary lymph nodes. The detection sensitivity of the mammaglobin RT-PCR is far superior to that of the CEA RT-PCR, allowing the diagnosis of occult metastases in nearly one-third of cases. Copyright © 2001 John Wiley & Sons, Ltd.

The etiology of inflammation, edema, and smoothmuscle contraction characteristic of inflammatory boweldisease is not clearly understood. There is evidencethat several neuropeptides, including substance P (SP), may play a role. In this study weevaluated the ability of a SP-antagonist (SR140333) tomodify the course of experimental colitis induced in therat by trinitrobenzene sulfonic acid (TNB). Colitis was induced in 24 rats using TNB applied byintrarectal enema. Twelve TNB-treated rats receivedSR140333, 0.1 mg/kg intraperitoneally, 30 min before theadministration of TNB and every 48 hr until death. Twelve rats receiving only intrarectal 0.9%saline served as controls. Rats of each group werekilled after 14 days. At day 14, the control groupshowed no signs of inflammation whereas the TNB-treated rats without SR140333 treatment exhibited awell-established colitis. The TNB-treated group had ahigher level of inflammation, as seen histologically andby the significantly greater weight of colon strips, compared to the controls (0.30 ± 0.09 gvs 0.13 ± 0.03 g, P < 0.001) and to theSR140333-treated rats (0.30 ± 0.09 g vs 0.14± 0.05 g, P < 0.001). In addition, smoothmuscle contractility was significantly reduced in the inflamedcolons of TNB-treated rats when compared with thecontrols (carbachol: 42.7 ± 20.3 vs 254.2± 69.78 mg/mm2± 10.02 vs 89.45± 23.17 mg/mm211.4 ± 2.2 vs 98.32 ± 33.57mg/mm21). However, SR140333-treated ratsshowed a recovery from inflammation and motoralterations caused by TNB (carbachol: 150.9 ±46.1 mg/mm21; SP: 32.5 ± 9.4 mg/mm25; KCl:125.7 ± 36.1 mg/mm21). In conclusion,treatment with SP antagonist SR140333 reduces theseverity of colitis and has beneficial effects on theconcomitant alterations of contractility. Thus, theblockade of substance P may represent a possibility inthe treatment of intestinal inflammation.

We report a case of necrotizing pneumonia due to Penicillium chrysogenum in a 57-year-old woman operated on for lung cancer. The residual right lower pulmonary lobe was infiltrated by Penicillium chrysogenum. The patient underwent a second pulmonary right lobectomy and was successfully treated with oral itraconazole. To our knowledge, this is the first case of pneumonia due to P. chrysogenum.