Infiltrative Lesions Research Articles

Effect of calcium-coacervate infiltration of artificial enamel caries lesions in de- and remineralizing conditions

ObjectivesCalcium-coacervate emulsions (CC) might be considered as mineral precursors to foster remineralization of carious dental hard tissues. This study analyzed the instant effect of repeated infiltration of artificial caries lesions with a CC emulsion as well as the effects of subsequent exposure of CC-infiltrated lesions to demineralizing and remineralizing environments. MethodsBovine enamel specimens were partly covered with varnish to leave three exposed windows. Artificial enamel caries lesions were created (pH 4.95, 17d). Baseline controls (BL) were obtained by preparing a thin section of each specimen. Specimens were allocated to five groups. In three groups lesions were etched with 37 % phosphoric acid gel, infiltrated with dipotassium hydrogen phosphate and subsequently with a calcium coacervate emulsion, prepared by mixing CaCl2 ⋅ 2H2O with polyacrylic acid sodium salt (PAA-Na). Subsequently, the infiltration effect was either analyzed immediately (Inf.) or after exposition to either de- (Inf.+DS) or remineralizing solution (Inf.+RS) for 10 or 20 days, respectively. In two control groups specimens were exposed to either DS or RS, respectively without prior CC infiltration. Integrated mineral loss [ΔZ(vol%×µm)] was analyzed using transverse microradiography (TMR). ResultsInfiltration of enamel caries lesions with coacervate solution resulted in only subtle immediate mineral gain even if repeated. When exposed to demineralizing conditions, infiltrated lesions showed significantly less mineral loss compared to untreated controls (p < 0.05; Kruskal Wallis) and exhibited characteristic mineral depositions within the lesion body. ConclusionsWhile immediate mineral gain by infiltration was only modest, the CC-emulsion might be able to prevent demineralization in acidic conditions. Clinical significanceCalcium coacervates might act protective against further demineralization when infiltrated into enamel caries lesions.

Neutrophilic leukocytosis and erythema nodosum leprosum in leprosy: insights from a retrospective observational study.

Leprosy reactions represent immunologically mediated episodes of acute inflammation that, if not diagnosed and treated promptly, can cause irreversible impairment of nerve function and permanent disabilities. A frequent type of reaction experienced by patients with lepromatous leprosy (LL) and borderline lepromatous leprosy (BL) is erythema nodosum leprosum (ENL), an inflammatory complication that may become chronic or recur in multiple episodes. Although ENL is commonly described as a neutrophil-mediated immune disease, the role of neutrophils is not fully understood. In this study, we assess neutrophilic leukocytosis in a retrospective cohort of patients affected by BL or LL leprosy. A retrospective observational study was performed using data from 146 patients with BL and LL leprosy diagnosed and treated at the Souza Araújo Outpatient Clinic, Fiocruz, Rio de Janeiro, Brazil. Clinical, demographic, and hematological data were extracted from medical records. Skin biopsy samples obtained from patients for ENL diagnosis were used for histopathological evaluations. Most patients were male (75%) and had a reactional episode (85%), of which 65% were ENL. Multiple episodes were common, 55% of the 80 patients with ENL presented more than 2 episodes (average of 2.6 episodes). In treatment-naive BL/LL patients, the median blood neutrophil counts of patients who developed ENL at some points of their disease course were higher than those who did not experience any reaction (median= 4,567 cells/mm3 vs 3,731 cells/mm3 respectively, p=0.0286). A correlation between the increase in median neutrophil counts and ENL severity was confirmed (6,066 cells/mm3 for mild ENL vs 10,243 cells/mm3 for moderate/severe ENL, p=0.0009). A longitudinal assessment was also performed in 34 patients, confirming the neutrophilic leukocytosis (BL/LL: 4896 cells/mm3 vs ENL: 8408 cells/mm3, p<0.0001). Moreover, increased NLR was associated with a greater neutrophilic infiltration in ENL lesions. We demonstrate that ENL episodes in patients affected by leprosy are associated with elevated blood leukocyte and neutrophil counts and an increased NLR. These findings highlight the significant involvement of neutrophils in the ENL immunological/inflammatory process.

Predictive nomogram for bone metastases in lung cancer based on monocyte infiltration.

The presence of bone metastases (BM) in patients with lung cancer is indicative of a worse prognosis. The present study aims to investigate the risk factors associated with BM in patients with lung cancer. Patients with lung cancer admitted to the First Affiliated Hospital of Anhui Medical University between June 2019 and September 2021 were enrolled in this study. A nomogram was constructed based on the outcomes derived from univariate and multivariate analyses. Concordance index, calibration plots, receiver operating characteristic curves, and decision curve analysis were used to evaluate the nomogram. To substantiate the influence of monocytes on lung cancer BM, various assays, including cell co-culture, Transwell, wound-healing assays, and immunohistochemistry and immunofluorescence staining, were conducted. Statistical analyses were performed using SPSS 22.0 software and GraphPad Prism 7.0. A total of 462 eligible patients were enrolled, comprising 220 with BM and 242 without. Multivariate analysis revealed that histological type, medical history, monocyte percentage, and LDH (Lactate Dehydrogenase) and ALP (Alkaline Phosphatase) levels were independent risk factors for BM in lung cancer. Transwell and wound-healing assays indicated that co-culture with monocytes significantly enhanced the migration and invasion capabilities of A549 cells in vitro. Immunohistochemistry and immunofluorescence analyses demonstrated a noteworthy increase in monocyte infiltration in the primary lesions of patients with lung cancer with BM. In conclusion, this study successfully constructed and validated a precise, straightforward, and cost-effective prognostic nomogram for patients with lung cancer with BM.

Cysteine Leukotriene Receptor Antagonist—Montelukast—Treatment Improves Experimental Abdominal Aortic Aneurysms in Mice

Background: Cysteinyl leukotrienes (LTs) and their receptors are involved in the pathogenesis of abdominal aortic aneurysms (AAAs). However, whether CysLT1 receptor antagonists such as montelukast can influence experimental nondissecting AAA remains unclear.Methods: Nondissecting AAAs were induced in C57BL/6J mice by transient aortic luminal infusion of porcine pancreatic elastase (PPE). All animals were administrated montelukast (1 or 10 mg/kg, daily) or vehicle by gavage beginning 1 day before PPE infusion for 14 days. On day 0 (baseline) and day 14 after PPE infusion, abdominal aortic diameters were directly measured. Aortic aneurysmal segment samples were collected, and histopathological analysis was performed.Results: Compared to vehicle treatment, montelukast significantly decreased PPE infusion–induced aortic expansion in a dose‐dependent manner (0.09‐mm reduction at a low dose and 0.19‐mm reduction at a high dose). Histopathological analysis also revealed that compared with vehicle treatment, montelukast treatment, especially in the high‐dose group, significantly improved PPE‐induced aortic elastin degradation and medial smooth muscle cell depletion. Both doses of montelukast also markedly decreased the number of local leucocytes, including macrophages, CD4+ T cells, CD8+ T cells, and B cells, infiltration and accumulation in aortic aneurysmal lesions. Montelukast treatment also downregulated matrix metalloproteinase 2 (MMP2) and MMP9 expression and inhibited mural angiogenesis in aneurysmal aortas.Conclusion: Montelukast treatment improves experimental nondissected AAAs in mice partly by improving aortic inflammation.

Sodium chloride promotes macrophage pyroptosis and aggravates rheumatoid arthritis by activating SGK1 through GABA receptors Slc6a12.

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by synovial inflammation and the production of autoantibodies. Previous studies have indicated an association between high-salt diets (HSD) and an increased risk of RA, yet the underlying mechanisms remain unclear. Macrophage pyroptosis, a pro-inflammatory form of cell death, plays a pivotal role in RA. In this study, we demonstrate that HSD exacerbates the severity of arthritis in collagen-induced arthritis (CIA) mice, correlating with macrophage infiltration and inflammatory lesions. Given the significant alterations observed in macrophages from CIA mice subjected to HSD, we specifically investigate the impact of HSD on macrophage responses in the inflammatory milieu of RA. In our in vitro experiments, pretreatment with NaCl enhances LPS-induced pyroptosis in RAW.264.7 and THP-1 cells through the p38 MAPK/NF-κB signaling pathway. Subsequent experiments reveal that Slc6a12 inhibitors and SGK1 silencing inhibit sodium-induced activation of macrophage pyroptosis and the p38 MAPK/NF-κB signaling pathway, whereas overexpression of the SGK1 gene counteracts the effect of sodium on macrophages. In conclusion, our findings verified that high salt intake promotes the progression of RA and provided a detailed elucidation of the activation of macrophage pyroptosis induced by sodium transportation through the Slc6a12 channel.

Gastric adenocarcinoma with intestinal progenitor cell differentiation: a morphologically underdiagnosed and more invasive distinctive type of gastric adenocarcinoma.

This study aims to explore the clinical and pathological characteristics, prognosis, diagnosis, and differential diagnosis of gastric adenocarcinoma with enteroblastic differentiation (GAED) in elderly patients. A total of 16 cases of GAED diagnosed from August 2019 to August 2022 at the First Affiliated Hospital of Nanchang University were retrospectively collected to analyze their clinical and pathological features. A control group of 360 cases of conventional gastric adenocarcinoma diagnosed during the same period was used for comparison. Among the 16 GAED patients, 11 were male and 5 were female, with ages ranging from 64 to 89 years (median age 75.5 years). Clinical manifestations of these patients included symptoms such as abdominal pain, bloating, hematemesis, and melena. The macroscopic classification revealed 11 cases of ulcerative lesions, 4 protruded lesions, and 1 diffusely infiltrative lesion. Tumor sizes varied from 3 to 9.5 cm in diameter, with a median diameter of 4.75 cm. Microscopically, the tumor cells exhibited tubular, papillary, and cribriform arrangements, with cuboidal or columnar morphology, relatively distinct cell boundaries, and cytoplasm that appeared clear or weakly acidophilic. Immunophenotyping analysis revealed the expression of SALL4 (15/16), Glypican-3 (12/16), CDX2 (12/16), CD10 (10/16), and p53 (12 cases exhibiting mutant expression, 4 cases exhibiting wild-type expression) within the tumor cells. There was no loss of mismatch repair proteins (MLH1, PMS2, MSH2, MSH6). The Ki-67 proliferation index ranged from 50% to 95%. In comparison to conventional gastric adenocarcinoma, GAED was frequently found in the gastric antrum (P<0.001) and exhibited a higher incidence of intravascular cancer emboli (P<0.001). Significant differences were noted in the Lauren classification, invasion depth, differentiation degree (P<0.01), and macroscopic type (P<0.05). However, no significant differences were found regarding age, gender, tumor diameter, neural invasion, or lymph node metastasis (P>0.05). The postoperative follow-up ranging from 5 to 29 months revealed one death and 15 cases of disease-free survival. GAED is a special subtype of gastric adenocarcinoma characterized by a combination of embryonal and intestinal differentiation immunophenotypes, as well as its increased propensity for biological invasion. Accurate identification of GAED is crucial in pathological practice, as it helps differentiate between GAED and conventional adenocarcinoma and aids in the evaluation of tumor malignancy. Furthermore, it is imperative to conduct a differential diagnosis that involves hepatoid adenocarcinoma, yolk sac tumor-like adenocarcinoma, and metastatic hepatocellular carcinoma.

Accidental Microcoil Migration into Right Atrium during Portal Vein Embolisation: A Case Report

With the advancement of technology in the field of medicine, minimally invasive vascular procedures are widely utilised for therapeutic effects. Embolisation is a minimally invasive approach to occlude a vessel for therapeutic benefit. However, these procedures are associated with a small percentage of complications, one of which is the migration of the embolising agent. Migration refers to the movement of the embolisation agent (mostly a coil) from the original placement site to an unwanted location. A 59-year-old male presented with complaints of abdominal pain lasting 2-3 months. A Contrast-enhanced Computed Tomography (CECT) scan of the abdomen revealed an ill-defined infiltrative lesion arising from the neck and body of the gallbladder. Curative surgery was planned in the form of an extended right hepatectomy; however, the Future Liver Remnant (FLR) calculated was not optimal (19%). The patient was therefore referred for preoperative Portal Vein Embolisation (PVE). During the procedure, there was an accidental microcoil migration to the right heart post-PVE, which was managed by minimally invasive techniques. The importance of multimodality imaging techniques used to identify the location and multidisciplinary approaches to aid management has also been highlighted.

Sarcoidosis Presented with Bilateral Trigeminal Neuropathy – A Case Report

Sarcoidosis is a multisystemic granulomatous disease of unknown origin, characterized by the presence of noncaseating granuloma in affected organs, and most frequently presented with bilateral hilar lymphadenopathy, pulmonary infiltration, skin and eye lesion. However, neurological involvement including peripheral neuropathy is relatively rare. Although the diagnosis of neurosarcoidosis can be challenging, electrophysiologic and laboratory evaluations suggestive of sarcoidosis lead to diagnosis of sarcoidosis. We report a patient who presented bilateral trigeminal neuropathies initially without other systemic symptoms or organ involvements.

Sarcoidosis Presented with Bilateral Trigeminal Neuropathy – A Case Report

Sarcoidosis is a multisystemic granulomatous disease of unknown origin, characterized by the presence of noncaseating granuloma in affected organs, and most frequently presented with bilateral hilar lymphadenopathy, pulmonary infiltration, skin and eye lesion. However, neurological involvement including peripheral neuropathy is relatively rare. Although the diagnosis of neurosarcoidosis can be challenging, electrophysiologic and laboratory evaluations suggestive of sarcoidosis lead to diagnosis of sarcoidosis. We report a patient who presented bilateral trigeminal neuropathies initially without other systemic symptoms or organ involvements.

The incidence rate and histological characteristics of intimal hyperplasia in elastase-induced experimental abdominal aortic aneurysms in mice.

Intimal hyperplasia (IH) is a negative vascular remodeling after arterial injury. IH occasionally occurs in elastase-induced abdominal aortic aneurysm (AAA) mouse models. This study aims to clarify the incidence and histological characteristics of IH in aneurysmal mice. A retrospective study was conducted by including 42 male elastase-induced mouse AAA models. The IH incidence, aortic diameters with or without IH, and hyperplasia lesional features of mice were analyzed. Among 42 elastase-induced AAA mouse models, 10 mice developed mild IH (24%) and severe IH was found in only 2 mice (5%). The outer diameters of the AAA segments in mice with and without IH did not show significant difference. Both mild and severe IH lesions show strong smooth muscle cell positive staining, but endothelial cells were occasionally observed in severe IH lesions. There was obvious macrophage infiltration in the IH lesions of the AAA mouse models, especially in mice with severe IH. However, only a lower numbers of T cells and B cells were found in the IH lesion. Local cell-secreted matrix metalloproteinases (MMP) 2 was highly expressed in all IH lesions, but MMP9 was only overexpressed in severe lesions. In conclusion, this study is the first to demonstrate the occurrence of aneurysmal IH and its histological characteristics in an elastase-induced mouse AAA model. This will help researchers better understand this model, and optimize it for use in AAA-related research.

Primary pulmonary T-cell lymphoma mimicking asthma and community-acquired pneumonia: a rare case report

Primary pulmonary T-cell lymphoma (PPTL) is a rare disease. Diagnosing PPTL is challenging due to non-specific clinical symptoms and imaging. A 32-year-old female presented with persistent fever, cough, and dyspnoea. The symptoms were initially treated as asthma and community-acquired pneumonia without improvement. Chest computed tomography (CT) revealed bilateral consolidations with a CT angiogram sign, and flexible bronchoscopy showed infiltrative lesions causing bronchial stenosis. Histopathological examination of the tissue biopsy identified T-cell lymphoma through immunohistochemical staining positive for CD3. This case highlights the importance of considering differential diagnoses such as PPTL in patients with atypical presentations of asthma or non-resolving pneumonia. This case also demonstrates the diagnostic utility of flexible bronchoscopy in identifying airway obstruction due to malignant cells, which can mimic asthma.

Clinical and imaging features of lymphomatosis cerebri: analysis of 8 cases and systematic review of the literature

Lymphomatosis cerebri (LC) is a rare type of primary central nervous system lymphoma with diffuse, nonenhancing infiltrative lesions and is often misdiagnosed. Our study aimed to investigate the clinical characteristics and prognosis of LC through analyzing patients from the literature and our own center, so as to improve early diagnosis and treatment. PubMed, Web of Science and our hospital databases were reviewed, and information on demographic, clinical, pathological, cerebrospinal fluid (CSF), neuroimaging and treatment options was extracted. Univariate survival analysis was conducted by generating survival curves and comparing them using the log-rank test. Multivariate analysis was performed using the Cox proportional hazards regression model to identify the prognostic predictors. A total of 81 patients (median age: 58 years; interquartile range, IQR: 50–66.5 years), 45 males and 36 females, were included. The most common symptoms were cognitive impairment (65.4%) and gait impairment (50.6%). Imaging studies indicated that all 81 patients had supratentorial structure involvement, and 93.8% (76/81) had bilateral hemisphere involvement. There were 53.3% (32/60) patients with CSF pleocytosis and 65% (39/60) patients with increased CSF protein levels. The median time of diagnosis was 4.8 months (IQR: 2.3–6.9 months). Compared with 4 (95% CI: 1.78–6.22) months for all 81 patients, the median OS was 20 (95% CI: 8.24–31.76) months for those who had chemotherapy plus radiotherapy. Multivariate Cox analysis revealed that chemoradiotherapy (HR: 0.12; 95% CI: 0.02–0.68) and higher CSF glucose level (HR: 0.01; 95% CI: 0.00–0.26) were inversely associated with death. The diagnosis of LC should be alerted when neuroimaging with bilateral hemispheric involvement and CSF abnormality with pleocytosis and increased protein. Once the diagnosis is confirmed, the combination of chemotherapy and radiotherapy can be considered if the patient’s physical condition permits.Journal standard instruction requires an unstructured abstract. Kindly check and confirm.We have checked and confirmed that there is no problem.

Th17-associated cytokines IL-17 and IL-23 in inflamed skin of Darier disease patients as potential therapeutic targets

Darier disease (DD) is a rare, inherited multi-organ disorder associated with mutations in the ATP2A2 gene. DD patients often have skin involvement characterized by malodorous, inflamed skin and recurrent, severe infections. Therapeutic options are limited and inadequate for the long-term management of this chronic disease. The aim of this study was to characterize the cutaneous immune infiltrate in DD skin lesions in detail and to identify new therapeutic targets. Using gene and protein expression profiling assays including scRNA sequencing, we demonstrate enhanced expression of Th17-related genes and cytokines and increased numbers of Th17 cells in six DD patients. We provide evidence that targeting the IL-17/IL-23 axis in a case series of three DD patients with monoclonal antibodies is efficacious with significant clinical improvement. As DD is a chronic, relapsing disease, our findings might pave the way toward additional options for the long-term management of skin inflammation in patients with DD.

Integrative network pharmacology and transcriptomics analysis reveal the mechanism of Tanreqing in the treatment of acne vulgaris

BackgroundAcne vulgaris is a common skin disease that affects the pilosebaceous unit, and inflammation plays an important role. Chinese traditional medicine Tanreqing (TRQ) has been used in the field of dermatology to treat inflammatory diseases and has shown outstanding efficacy. The purpose of this study was to evaluate the potential advantages of TRQ on a mouse model of acne inflammation. Additionally, network pharmacology and transcriptome analysis were utilized to investigate the possible underlying mechanisms. MethodsThe active compounds of TRQ were collected through TCMSP database and literature review, and the predicted targets of active compounds were obtained from Swiss Target Prediction. Acne targets were collected from the Gene Cards database and DisGeNET. Cytoscape v3.7.1 was used to build the "compounds-targets" network and PPI network and to obtain the core network. GO analysis and KEGG pathway annotation were performed on the core genes. The Illumina HiSeq sequencing platform was utilized to sequence mRNA from mouse skin tissue in acne areas. Differential gene expression analysis was conducted to identify genes that were affected by TRQ, and their associated biological functions and signaling pathways were analyzed. The transcriptomic and network pharmacology analyses were integrated to generate predictive results. Additionally, the efficacy of TRQ in treating acne was confirmed through H&E staining, and the predicted outcomes were verified through quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). ResultsThe study's results indicate that 37 potential target genes were enriched in multiple signaling pathways, including the atherosclerosis, IL-17, and TNF signaling pathways, according to network pharmacology. In addition, 338 transcriptomic DEGs were found to be involved in various signaling pathways, including Cell adhesion molecules and the IL-17 signaling pathway.The combined analysis of these findings suggests that the IL-17 and TNF signaling pathways are the primary mechanisms by which TRQ exerts its anti-acne effects. H&E staining revealed that TRQ inhibited inflammatory cell infiltration in acne lesions and attenuated the inflammatory response in acne. Moreover, TRQ significantly suppressed key factors such as TNF-α, JNK2, IL-17A, C/EBPβ, IL-6, and IL-1β in the IL-17 and TNF signaling pathways. Furthermore, TRQ also demonstrated a significant inhibition in the expression of TNF-α and IL-1β in the skin tissues of acne vulgaris mice ConclusionOur findings suggest that TRQ may effectively inhibit the IL-17/TNF signaling pathway by suppressing the expression of TNF-α and IL-1β, making it a potential candidate for the treatment of acne

Keratinocyte FABP5-VCP complex mediates recruitment of neutrophils in psoriasis

One of the hallmarks of intractable psoriasis is neutrophil infiltration in skin lesions. However, detailed molecular mechanisms of neutrophil chemotaxis and activation remain unclear. Here, we demonstrate a significant upregulation of epidermal fatty acid binding protein (E-FABP, FABP5) in the skin of human psoriasis and psoriatic mouse models. Genetic deletion of FABP5 in mice by global knockout and keratinocyte conditional (Krt6a-Cre) knockout, but not myeloid cell conditional (LysM-Cre) knockout, attenuates psoriatic symptoms. Immunophenotypic analysis shows that FABP5 deficiency specifically reduces skin recruitment of Ly6G+ neutrophils. Mechanistically, activated keratinocytes produce chemokines and cytokines that trigger neutrophil chemotaxis and activation in an FABP5-dependent manner. Proteomic analysis further identifies that FABP5 interacts with valosin-containing protein (VCP), a key player in NF-κB signaling activation. Silencing of FABP5, VCP, or both inhibits NF-κB/neutrophil chemotaxis signaling. Collectively, these data demonstrate dysregulated FABP5 as a molecular mechanism promoting NF-κB signaling and neutrophil infiltration in psoriasis pathogenesis.

Blockade of IL-18Rα-mediated signaling pathway exacerbates neutrophil infiltration in imiquimod-induced psoriasis murine model.

Psoriasis is an immune-mediated inflammatory disease of the skin, which is characterized by epidermal hyperkeratosis and neutrophil infiltration. The interleukin (IL)-17/IL-23 pathway and associated cytokines play major roles in the pathogenesis and exacerbation of psoriasis. The IL-18/IL-18 receptor (R) α signaling pathway is important for Th1 cytokine production and differentiation of Th1 cells; however, its role in the pathogenesis of psoriasis remains unknown. In this study, we investigated the effect of the IL-18Rα-mediated signaling pathway in the pathogenesis of psoriasis in Il18ra-deficient mice (Il18ra-/-) and wild-type imiquimod (IMQ)-induced psoriatic dermatitis model mice. Blocking this pathway exacerbated IMQ-induced psoriatic skin inflammation. Il18ra deficiency led to significant increases in the levels of IL-1β, IL-6, IL-8, IL-17A, IL-23, and chemokine (C-X-C motif) ligand 2 in skin lesions. Gr1-positive cells highly infiltrated psoriatic skin lesions in Il18ra-/- mice compared to those in wild-type mice. Citrullinated histone H3-positive area was relatively broad in Il18ra-/- mice. These results suggest that IL-18Rα-mediated signaling pathways may inhibit psoriatic skin inflammation by regulating infiltration and activation of neutrophil and other innate immune cells.

Paediatric thoracic actinomycosis presenting as back swelling: A case report

Presentation: A seven years old girl presented with a three-day history of cough and fever, and several weeks of back pain, anorexia and weight loss. Examination was significant only for a tender, non-erythematous swelling to the right mid-back measuring ten centimetres in length. Diagnosis and treatment: Investigations on admission included neutrophilia and elevated inflammatory markers. Chest radiograph demonstrated a confluent area of opacification within the right peripheral lower zone with a small pleural effusion. CT reported two large enhancing and infiltrative lesions in the right thorax and the right posterior lower ribs, and disseminated lymphadenopathy. Microbiology and histology of a tissue sample were conclusive for actinomycosis israelii. She had a full recovery following a nine month course of oral amoxicillin. Discussion: Invasive actinomycosis is rare, and a high clinical suspicion and thorough investigation is warranted with invasive pneumonia and atypical associated symptoms. Keywords: Actinomycosis; Pneumonia; Chest wall mass; non-accidental injury.

Epidemiologic, clinical and therapeutic features of primary cutaneous lymphomas in Morocco

AbstractBackgroundFew epidemiological studies on primary cutaneous lymphomas are available and related to limited populations.ObjectivesTo characterize the epidemiologic, clinical and therapeutic features of primary cutaneous lymphomas from a global perspective at the national level.MethodsA cross‐sectional descriptive multicenter study including patients treated for cutaneous lymphomas at dermatology and venereology departments of different university hospitals in the kingdom of Morocco from January 2012 to December 2021.ResultsOur multicenter cohort consisted of 402 patients. The median age was 56 years (15–114) with a male predominance (61%, 245 cases). Based on the WHO‐EORTC classification, the most frequent histological type was cutaneous T‐cell lymphoma (CTCL) (88% of cases). Of these, mycosis fungoides (MF) was the most common (78%). B‐cell lymphomas represented 12% of cases, mainly centro‐follicular B‐cell lymphoma (40%). The clinical presentation was most frequently erythematous and scaly infiltrated lesions in 187 CTCL patients (52.6%), and nodular lesions in 37 patients (78%) with B‐cell lymphomas. Treatment modalities depended on the tumour's histological type and stage and included: topical corticosteroids and phototherapy in 52% of cases, monochemotherapy, radiotherapy, photopheresis and polychemotherapy. The evolution was marked by remission in 41% of patients, relapse in 17% and death in 12%.ConclusionsOur national study provides data on primary cutaneous lymphomas in Morocco, never before mentioned in indexed literature. We identified 402 cases over a 10‐year period. A better knowledge of these entities is key to optimize diagnosis and therapy.

Spontaneous Primary Pneumothorax as A Complication of Neurofibromatosis Type 1.

NF1 is a genetic disease that results in cutaneous conditions, including neurofibroma, axillary, inguinal lentigines and café au lait spots. In some cases (5-20%) it can also affect the lungs, causing neurofibroma, infiltrative and cystic lesions, emphysema or bullae, leading to chronic respiratory failure.SSP is a clinical presentation of NF1 caused by the rupture of lung cysts or bullae, with an unclear relationship to smoking.Early diagnosis of pulmonary manifestations in patients with NF1 is crucial as surgical removal of lung cysts and bullae seems to prevent recurrence of SSP.

Analysis of microbiota reveals the underlying mechanism of PHF11 in the development of Enterococcus-regulated endometriotic cysts

Endometriosis (EMS) is a prevalent disease and the etiologies has not uniform. Microbiota is associated with human diseases. To delve into the relationship between EMS and microbiota, Ectopic (EM) and eutopic (EU) endometrial tissues, pharyngeal swabs, and stools were collected from EMS patients. The microbiota composition of EM and EU partially overlapped, with similar taxon numbers and diversity, but the richness levels were significantly different. A comparison of intestinal microbes in healthy individuals (FN) and EMS patients (FE) revealed that the richness of Enterococcus, Pseudomonas, Haemophilus, and Neisseria was enhanced in FE. In addition, Enterococcus-induced mice (EFA) presented with a higher degree of lesion infiltration and a wider distribution of lesions. Proteomic analysis revealed the expression of plant homeodomain finger 11 (PHF11) was notably downregulated in EFA. And the downregulated expression of PHF11 was accompanied by the upregulated expression of interleukin 8 (IL-8). Our findings suggest a potential regulatory mechanism for PHF11 in EMS development.