Histological Manifestations Research Articles

Hereditary Multiple Intestinal Atresia With a Novel TTC7A Pathogenic Variant: Gastrointestinal Manifestations in Two Cases.

Hereditary multiple intestinal atresia (HMIA) with TTC7A mutation is caused by homozygous or compound heterozygous TTC7A gene mutation. It is characterized by multiple small and large intestinal atresias and/or stenoses. TTC7A mutation is described in some patients with inflammatory bowel disease and mild-severe forms of severe combined immunodeficiency without intestinal atresia or stenosis. We present 2 cases of intestinal atresia and documented TTC7A mutation with a novel variant. Both cases had different clinical and pathological manifestations. The first case is a male infant born at 35 weeks of gestation with failure to pass meconium. Intestinal biopsy reveals apoptotic enteropathy with villous atrophy and increased mucosal eosinophils. The second case is referred at birth for antenatally detected umbilical hernia, polyhydramnios and possible upper intestinal obstruction. The resected specimen reveals ileal atresia with partial villous atrophy, decreased number of lamina propria inflammatory cells and absence of plasma cells. In conclusion, these cases reflect an emerging TTC7A pathogenic variant with different histological manifestations and leads to characterization as immune dysregulation disorder. There is a need to differentiate TTC7A mutation associated ones from cases labeled as very early onset IBD and rule out other hereditary immunodeficiencies.

Testicular and Paratesticular Neoplasms in Pediatrics: Report of 5 Cases with Atypical Presentation and Literature Review

This study presents 5 atypical cases of testicular and paratesticular neoplasms in pediatrics, highlighting the importance of a high level of clinical suspicion and accurate diagnostic approach. Although rare, these neoplasms can present a variety of clinical and histological manifestations, complicating their diagnosis. Early recognition and proper classification are crucial to ensure effective treatment and a favorable prognosis. Multidisciplinary collaboration, including oncology, pediatric surgery, and endocrinology, is essential to address the oncological and developmental needs of patients. The study concludes that rigorous clinical vigilance and a multidisciplinary approach are fundamental in addressing these challenges in pediatric care for patients with testicular and paratesticular neoplasms.

Cancer therapy-related interstitial lung disease.

With the increasing utilization of cancer therapy, the incidence of lung injury associated with these treatments continues to rise. The recognition of pulmonary toxicity related to cancer therapy has become increasingly critical, for which interstitial lung disease (ILD) is a common cause of mortality. Cancer therapy-related ILD (CT-ILD) can result from a variety of treatments including chemotherapy, targeted therapy, immune checkpoint inhibitors, antibody-drug conjugates, and radiotherapy. CT-ILD may progress rapidly and even be life-threatening; therefore, prompt diagnosis and timely treatment are crucial for effective management. This review aims to provide valuable information on the risk factors associated with CT-ILD; elucidate its underlying mechanisms; discuss its clinical features, imaging, and histological manifestations; and emphasize the clinical-related views of its diagnosis. In addition, this review provides an overview of grading, typing, and staging treatment strategies used for the management of CT-ILD.

Role of gut microbiota in Crohn's disease pathogenesis: Insights from fecal microbiota transplantation in mouse model.

Inflammatory bowel disease, particularly Crohn's disease (CD), has been associated with alterations in mesenteric adipose tissue (MAT) and the phenomenon termed "creeping fat". Histopathological evaluations showed that MAT and intestinal tissues were significantly altered in patients with CD, with these tissues characterized by inflammation and fibrosis. To evaluate the complex interplay among MAT, creeping fat, inflammation, and gut microbiota in CD. Intestinal tissue and MAT were collected from 12 patients with CD. Histological manifestations and protein expression levels were analyzed to determine lesion characteristics. Fecal samples were collected from five recently treated CD patients and five control subjects and transplanted into mice. The intestinal and mesenteric lesions in these mice, as well as their systemic inflammatory status, were assessed and compared in mice transplanted with fecal samples from CD patients and control subjects. Pathological examination of MAT showed significant differences between CD-affected and unaffected colons, including significant differences in gut microbiota structure. Fetal microbiota transplantation (FMT) from clinically healthy donors into mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD ameliorated CD symptoms, whereas FMT from CD patients into these mice exacerbated CD symptoms. Notably, FMT influenced intestinal permeability, barrier function, and levels of proinflammatory factors and adipokines. Furthermore, FMT from CD patients intensified fibrotic changes in the colon tissues of mice with TNBS-induced CD. Gut microbiota play a critical role in the histopathology of CD. Targeting MAT and creeping fat may therefore have potential in the treatment of patients with CD.

Chronic pyogenic spondylitis in patients with spinal gout: a case series and literature review

Background. Spinal gout is a rare and poorly described group of noninfectious inflammatory spinal lesions characterized by the deposition of monosodium urate crystals in the epidural space, paravertebral soft tissues, and by facet joints damage. There is no systematized data on the course of infectious spondylitis and spinal gout in the literature. The aim of the study — to present long-term outcomes of surgical treatment of chronic pyogenic spondylitis in patients with spinal gout and systematize the literature data on the issue. Methods. The clinical part of the study included 6 consecutively operated patients in the period from 2018 to 2021. The diagnosis of spinal gout and chronic pyogenic spondylitis was verified according to the results of histologic and bacteriologic studies of surgical material. Catamnesis accounted for at least 12 months. We studied the peculiarities of clinical and laboratory, radiological and histologic manifestations of the disease. Literature data systematization was carried out in the databases PubMed, Google Scholar, eLIBRARY from 2013 to 2023. Inclusion criteria: level of evidence II B-IV, catamnesis more or equal to 6 months, information on diagnostic and treatment measures. Results. The average age of the patients was 55±9 years. The duration of the diagnostic pause was 8±5 years. Multisegmented lesions of the lumbar (n = 6) spine prevailed. According to the classification of Pola E. et al. (2017) the following types of spondylitis were identified: B.3 (n = 1), C.1 (n = 1), C.3 (n = 2) and C.4 (n = 2). The clinical manifestation was dominated by chronic back pain with an intensity of 6,1±1,4 VAS scores. Neurologic disorders of the lower extremities and pelvic (ASIA scale) corresponded to types B (n = 1) and C (n = 4). The type of surgery: three-column reconstruction through combined approach in 2 cases and isolated anterior column reconstruction in 2 cases, 360° fusion in 1 case, and debridement of the epidural space and anterior column through posterior approach in 1 case. The follow-up results show the absence of recurrence of spondylitis in 4 cases, in 2 patients there were postoperative complications that required revision, after which no recurrence of spondylitis was noted. We selected 17 publications for literature review. Conclusion. The combination of chronic pyogenic spondylitis and spinal gout is a rare and poorly described pathology in the literature. Long therapeutic pause, chronic character of vertebrogenic pain syndrome in combination with increased uric acid level and formation of tophi of vertebral localization are distinctive features of the disease. Neurologic disorders with the combination of spondylitis and gout result from stenosis of the spinal canal due to two factors — epidural abscesses and tophi. Achieving local control of the combined pathology is possible with a combination of surgical intervention and long-term administration of hypouricemic drugs.

The β2-adrenergic receptor agonist formoterol attenuates necrosis and apoptosis in the rat myocardium under experimental stress-induced cardiac injury.

Currently, there is no effective therapy for takotsubo syndrome (stress-induced cardiac injury in humans) in the clinics. It has previously been shown that β2-adrenergic receptor (β2-AR) agonist formoterol reduces cardiomyocyte injury in experimental takotsubo syndrome. The aim of this study was to investigate whether formoterol prevents apoptosis and necrosis of cardiomyocytes and endothelial cells in stress-induced cardiomyopathy. Stress-induced cardiac injury was induced by immobilization of rats for 2, 6, and 24 hours. The myocardium of stressed rats showed a reduction in contractility and histological manifestations of cardiomyocyte damage: karyopyknosis, perinuclear edema of cardiomyocytes and endothelial cells, and microcirculation disturbances augmented with extended exposure to stress. In addition, apoptosis of endothelial cells was detected 6hours after the onset of stress and peaked at 24 hours. Apoptosis of cardiomyocytes significantly gained only after 24 hours of stress exposure. These morphological alterations were associated with increased levels of serum creatine kinase-MB, syndecan-1, and thrombomodulin after 24 hours of stress. Administration of β2-AR agonist formoterol (50 μg/kg) four times during 24-hour stress exposure led to the improvement in myocardial inotropy, decrease in the severity of histological signatures, reduction in the number of TUNEL-positive cardiomyocytes, serum creatine kinase-MB, syndecan-1, and thrombomodulin levels. Present data suggest that apoptosis and necrosis of cardiomyocytes and necrosis of endothelial cells in stress-induced cardiac injury can be mitigated by activation of the β2-AR. However, formoterol did not eliminate completely cardiomyocyte apoptosis, histological alterations, or endothelium injury markers under stress.

Suppression of STK39 weakens the MASLD/MASH process by protecting the intestinal barrier.

STK39 is reportedly a critical negative regulator of intestinal barrier. Pharmacological targeting of STK39 is expected to protect the intestinal barrier and thereby weaken metabolic dysfunction-associated steatohepatitis (MASH); Proximal colon biopsy tissues from patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and those without MASLD were analyzed for STK39 expression. Wildtype (WT) mice and systemic STK39 gene knockout (STK39-/-) male mice were fed a normal diet or a high-fat methionine-choline deficient diet (HFMCD) for 8 weeks. The MASH mice were grouped and treated with ZT-1a (a STK39 inhibitor) or vehicle intraperitoneal injection during the procedure of HFMCD induction. Liver and intestinal tissues were collected for further examination; Colon tissues from patients with MASLD exhibited higher levels of STK39 than those from subjects without MASLD. Knockout of STK39 diminished CD68+ Kupffer cells and α-SMA+ hepatic stellate cells infiltration in mouse MASH model. Treatment with ZT-1a also prevented severe steatohepatitis in a mouse MASH model, including milder histological and pathological manifestations (lobular inflammation and fibrosis) in the liver. Interestingly, Inhibition of STK39 had minimal effects on hepatic lipid metabolism. The reduced liver injury observed in mice with STK39 inhibition was linked to significant decreases in mucosal inflammation, tight junction disruption and intestinal epithelial permeability to bacterial endotoxins; Collectively, we have revealed that inhibiting STK39 prevents the progression of MASH by protecting the intestinal epithelial barrier.

A Review of Atypical Cutaneous Histological Manifestations of Herpes Zoster.

The clinical and histopathological features of herpes zoster (HZ) are usually straightforward. Atypical histological presentations, in the absence of the classical viral cytopathic changes, are well documented and can make the diagnosis of HZ extremely difficult. Herein, we review the existing literature on atypical cutaneous histological manifestations of the disease, with emphasis on the subtle clues, use of immunohistochemistry, and potential pitfalls.

Morular Metaplasia of the Endometrium: A Case Report and Literature Review: Care Pathways based on Molecular Biology

Background: Endometrial morular metaplasia, a clinical conundrum from a diagnostic and management angle given its rarity and low oncogenic potential has been linked to endometrial hyperplasia and carcinoma. Case report: A 77-year-old woman with no significant past medical history was found to have an asymptomatic thickened endometrium on pelvic imaging, after presenting with lower abdominal pain, 3 yrs ago. Diagnostic hysteroscopy identified an endometrial polyp within a pyometra. Histopathology showed focal complex hyperplasia without atypia with superimposed morular metaplasia (EMM) amongst negative microbiology. Following conservative management with a Multidisciplinary Team (MDT) overview, as per her choice with 6-monthly follow-up hysteroscopies, endometrial biopsies, and a short use of the Mirena IUS (discontinued due to poor tolerance), histopathology shows resolved hyperplasia with persistent EMM. She is considering a hysterectomy. Discussion: Current evidence suggests that a sub-type of EMM, a likely histological manifestation of beta-catenin (CTNNB1) gene mutation: could be a precursor of endometrial hyperplasia and low-grade endometrioid-endometrial carcinoma sub-type. Though low-grade in nature, the increased recurrence risk raises significant concerns. Management options which include conservative, hormonal, and surgery have been described in the literature. A few cases of premenopausal women have been managed conservatively, with one resulting in a pregnancy. However, due to the lack of a natural history timeline, the optimal frequency of endometrial sampling when uterine-sparing, is unclear, leading to a management conundrum. Conclusion: Management of morular endometrial metaplasia can be difficult but must reflect the woman’s choice with an MDT overview. Immuno-histochemical tools utilizing new molecular biological advances can simplify the diagnostic and prognostication processes, aiding clinical management.

Histological manifestations of the Cervix with Chronic Cystic Cervicitis and Nabothian Cyst: Case Report

Nabothian cysts are non-malignant lesions that occur on the cervix and affect a large percentage of reproductive aged women. They usually occur because of childbirth or minor trauma; most of the time, they are small and asymptomatic and require no treatment. However, large nabothian cysts may vary in appearance and even resemble malignant tumors. Consequently, in order to rule out malignancy, a biopsy is advised. The greatest valuable imaging modalities for cervical cystic lesions are MRI and transvaginal ultrasonography. Nabothian cysts usually don't need any treatment, but if the lesion's nature is unclear and it hurts, surgery may be necessary. In this case study, chronic pelvic pain is described and abnormal uterine bleeding needed surgical intervention because of chronic cystic cervicitis and multiple nabothian cysts accompanied with Leiomyoma accompanied with adenomyosis and endometrial hyperplasia without atypia.

Identification and characterization of a novel strain of Decapod hepanhamaparvovirus in black tiger shrimp (Penaeus monodon) from Madagascar that does not cause histological lesions

Decapod hepanhamaparvovirus (DHPV) is a single-stranded DNA virus that primarily affects the early life stages of penaeid shrimp, potentially leading to significant losses in hatchery operations. In an interesting finding, we observed that a small portion Black tiger shrimp (Penaeus monodon) originating from Madagascar harbored DHPV even in the absence of any discernible clinical signs. Detailed histopathological analysis of P. monodon post-larvae individuals revealed an absence of distinctive histological lesions typically associated with DHPV infection. However, sensitive molecular techniques, including PCR and real-time PCR and reverse transcriptase quantitative PCR (RT-qPCR) confirmed the presence of viral DNA and DHPV encoded transcripts in these specimens. The complete genome sequence of this newfound viral isolate, spanning 6254 nucleotides, showed a 96.9% nucleotide sequence similarity to a previously documented DHPV strain also originating from Madagascar. Moreover, it exhibited a genetic resemblance of 80.7% to 88.2% when compared to DHPV strains from other geographical regions. These findings underscore the unique genomic and histological characteristics of this novel DHPV isolate. This knowledge proves to be of paramount significance for the screening of broodstock and post-larvae in captive breeding programs, as it aids in identifying the presence of DHPV. Furthermore, it paves the way for future investigations into unraveling the precise role of viral-encoded proteins in shaping the clinical and histological manifestations of DHPV infections.

Digital pathology and spatial omics in steatohepatitis: Clinical applications and discovery potentials.

Steatohepatitis with diverse etiologies is the most common histological manifestation in patients with liver disease. However, there are currently no specific histopathological features pathognomonic for metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, or metabolic dysfunction-associated steatotic liver disease with increased alcohol intake. Digitizing traditional pathology slides has created an emerging field of digital pathology, allowing for easier access, storage, sharing, and analysis of whole-slide images. Artificial intelligence (AI) algorithms have been developed for whole-slide images to enhance the accuracy and speed of the histological interpretation of steatohepatitis and are currently employed in biomarker development. Spatial biology is a novel field that enables investigators to map gene and protein expression within a specific region of interest on liver histological sections, examine disease heterogeneity within tissues, and understand the relationship between molecular changes and distinct tissue morphology. Here, we review the utility of digital pathology (using linear and nonlinear microscopy) augmented with AI analysis to improve the accuracy of histological interpretation. We will also discuss the spatial omics landscape with special emphasis on the strengths and limitations of established spatial transcriptomics and proteomics technologies and their application in steatohepatitis. We then highlight the power of multimodal integration of digital pathology augmented by machine learning (ML)algorithms with spatial biology. The review concludes with a discussion of the current gaps in knowledge, the limitations and premises of these tools and technologies, and the areas of future research.

Pulmonary Hypertension Secondary to Myxomatous Mitral Valve Disease in Dogs: Current Insights into the Histological Manifestation and Its Determining Factors

Pulmonary venous hypertension (PVH) is caused by deteriorating left ventricular function. The most common cause of PVH in dogs is myxomatous mitral valve degeneration (MMVD). It causes left ventricular volume overload and an increase in left atrial and pulmonary venous pressure (PVH), which leads to pulmonary vascular wall remodeling and contributes to the perpetuation and worsening of PVH. Pulmonary vascular wall remodeling is also characteristic of pulmonary arterial hypertension (PAH). However, the changes in PVH arise secondary to heart failure and vascular remodeling progresses as the disease progresses. On the other hand, PAH is a primary disease that can be triggered, for example, by the use of certain drugs. Similar structural changes may suggest the influence of similar pathophysiological mechanisms or the intermediation of similar mediators. Therefore, this article discusses recent and hitherto uncommented findings elucidating the pathophysiology of the processes and influences on the pattern of histological changes observed in pulmonary hypertension secondary to degenerative mitral valve disease. In particular, we focus on the activity of factors such as endothelin, serotonin, and nitric oxide, which are involved in pulmonary vascular wall remodeling in both PVH and PAH.

Sodium butyrate alleviates experimental autoimmune prostatitis by inhibiting oxidative stress and NLRP3 inflammasome activation via the Nrf2/HO-1 pathway.

Chronic prostatitis and chronic pelvic pain syndrome (CP/CPPS) leads to severe discomfort in males and loss of sperm quality. Current therapeutic options have failed to achieve satisfactory results. Sodium butyrate (NaB) plays a beneficial role in reducing inflammation, increasing antioxidant capacities, and improving organ dysfunction; additionally NaB has good safety prospects and great potential for clinical application. The purpose of the current research was to study the effect of NaB on CP/CPPS and the underlying mechanisms using a mouse model of experimental autoimmune prostatitis (EAP) mice. The EAP mouse model was successfully established by subcutaneously injecting a mixture of prostate antigen and complete Freund's adjuvant. Then, EAP mice received daily intraperitoneal injections of NaB (100, 200,or 400 mg/kg/day) for 16 days, from Days 26 to 42. We then explored anti-inflammatory potential mechanisms of NaB by studying the effects of Nrf2 inhibitor ML385 and HO-1 inhibitor zinc protoporphyrinon prostate inflammation and pelvic pain using this model. On Day 42, hematoxylin-eosin staining and dihydroethidiumstaining were used to evaluate the histological changes and oxidative stress levels of prostate tissues. Chronic pelvic pain was assessed by applying Von Frey filaments to the lower abdomen. The levels of inflammation-related cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor were detected by enzyme-linked immunosorbent assay. The regulation of Nrf2/HO-1 signaling pathway and the expression of NLRP3 inflammasome-related protein in EAP mice were detected by western blot analysis assay. Compared with the EAP group, chronic pain development, histological manifestations, and cytokine levels showed that NaB reduced the severity of EAP. NaB treatment could inhibit NLRP3 inflammasome activation. Mechanism studies showed that NaB intervention could alleviate oxidative stress in EAP mice through Nrf2/HO-1 signal pathway. Nrf2/HO-1 pathway inhibitors can inhibit NaB -mediated oxidative stress. The inhibitory effect of NaB on the activation of NLRP3 inflammasome and anti-inflammatory effect can also be blocked by Nrf2/HO-1 pathway. NaB treatment can alleviates prostatic inflammation and pelvic pain associated with EAP by inhibiting oxidative stress and NLRP3 inflammasome activation via the Nrf2/HO-1 pathway. NaB has the potential as an effective agent in the treatment of EAP.

Shave Excision Of Marginal Lower Eyelid Nevus

Introduction : INTRODUCTION: Nevus is a common benign melanocytic lesion and may appear in palpebral region. It may appear congenitally or acquired. Such lesions contain melanocyte derived from neural crest. Palpebral nevus is a group of heterogenous lesion with varying clinical and histological presentation depending on age and nevus stage. PURPOSE: To report shave excision procedure of the left inferior palpebral nevus located in the palpebral margin using local anesthesia.
 Case Illustration : CASE REPORT: A 43-years old woman came to the hospital with a solitary mass in the lower right eyelid. The mass was experienced since 2 year ago and slowly increasing in size and most notably 3 months prior. The mass was round, tender, painless, black-greyish colored, with a smooth surface, mobile, and measured 0,5 cm x 0,5 cm in size. The lesion was located in the middle portion of right lower palpebral margin without extension to the tarsal or bulbar conjunctiva. No bleeding or discharge was found. No history of trauma, use of medication, family history, previous ocular and systemic disease was found. Histopathological examination concluded the lesion was nevus pigmentosus. The nevus was excised entirely using shave excision technique with local anesthesia. Follow-up examination revealed an excellent result with no complications.
 Discussion : 
 Conclusion : CONCLUSION: Palpebral nevus pigmentosus are common benign tumor with wide range of clinical and histological manifestation. Not all palpebral nevus required surgical intervention. The most effective treatment is complete excision of the nevus and recurrence rate is generally low.

Increased neutrophil-derived IL-17A identified in generalized pustular psoriasis.

Generalized pustular psoriasis (GPP) is considered to be a distinct clinical entity from psoriasis vulgaris (PV), with different clinical and histological manifestations. The pathogenesis of GPP has not been thoroughly elucidated, especially in those patients lacking interleukin (IL)36RN. In present study, we performed RNA sequence analysis on skin lesions from 10 GPP patients (4 with and 6 without IL36RN mutation) and 10 PV patients without IL36RN mutation. Compared with PV, significantly overexpressed genes in GPP patients were enriched in IL-17 signalling pathway (MMP1, MMP3, DEFB4A and DEFB4B, etc.) and associated with neutrophil infiltration (MMP1, MMP3, ANXA and SERPINB, etc.). GPP with IL36RN mutations evidenced WNT11 upregulation and IL36RN downregulation in comparison to those GPP without IL36RN mutations. The expression of IL-17A/IL-36 in skin or serum and the origin of IL-17A in skin were also investigated. IL-17A expression in skin was significantly higher in GPP than PV patients, whereas, there were no differences in skin IL-36α/IL-36γ/IL-36RA or serum IL-17A/IL-36α/IL-36γ between GPP than PV. Besides, double immunofluorescence staining of MPO/IL-17A or CD3/IL-17A further confirmed that the majority of IL-17A in GPP skin was derived from neutrophils, but not T cells. These data emphasized the role of neutrophil-derived IL-17A in the pathogenesis of GPP with or without IL36RN mutations. Targeting neutrophil-derived IL-17A might be a promising treatment for GPP.

MgO Nanoparticle Synthesis, Chemical Delivery in Rat Model Induced Lung Injury

Acute lung injury is a disorder of acute inflammation that causes disruption of the lung endothelial and epithelial barriers. Acute Respiratory Distress Syndrome or ARDS is a diffuse inflammatory lung process that frequently manifests in critically ill patients, with an estimated incidence of 3 million people a year. Clinically, ARDS is manifested by bilateral or diffuse radiographic infiltrates, hypoxemia, decreased lung compliance, and increased ventilatory dead space. The histological manifestation of ARDS is diffuse alveolar damage as defined by epithelial injury, hyaline membrane formation and alveolar flooding with proteinaceous fluid, increase alveolar surface area and frequently neutrophilic inflammation. The animal model correlate to ARDS as an acute lung injury (ALI). Models were employed to test potential new therapeutic interventions and to investigate under-lying mechanistic pathways that lead to diffuse lung injury. In this study cage cigarette smoke model was used for an acute lung injury. For that purpose, thirty (30) young albino healthy rats were used, and their duration of trial was 21 days. Each group was given an oral drug administration containing MgO-150mg/kg, MgO-300mg/kg BW for treatment and diet schedule in young albino rats of male sex for the experimental procedure of 0 to 21 days. Mean body weight, BALF, lipid profile, liver profile and lung histology were assessed. Results revealed that MgO nanoparticles exhibited antioxidant capacity at dosages of 300mg/kg, and 150mg/kg. This formulation of selected nanoparticles at high dose exhibited an acute lung injury and antioxidant effects as compared to low dose extract. Additionally, transcriptional factors revealed up-regulation at high dose in contrast to the low dose extract in lung injury treated groups.

Ptychotropic porokeratosis (porokeratosis ptychotropica): features of clinical and histological manifestations

Ptychotropic porokeratosis (porokeratosis ptychotropica): features of clinical and histological manifestations

Gastroprotective effect of Vien Khoi Tim capsules on indomethacin-induced gastric ulcers in rats

Available anti-ulcer drugs unveil partial effectiveness and numerous adverse reactions. Plants offer an alternative strategy in the search for new drugs in the therapy and prevention of peptic ulceration. The present study investigated the possible protective effect of the herbal formulation Vien Khoi Tim (VKT) on indomethacin-induced gastric mucosal damage in rats. VKT was tested at two doses (1.44 & 0.48 capsules/kg/d po) ten days before the indomethacin single-dose challenge (40 mg/kg po). Animals were sacrificed six hours after indomethacin administration, and gastric tissues were collected for gross observation and histopathological analyses. The results revealed that the administration of indomethacin caused evident gastric mucosal damage with morphological and histological manifestations. VKT pretreatment tended to avert the rise in lesion numbers, reduce the ulcer index, and improve the severity of bleeding streaks and epithelial sloughing in gastric mucosa on the macroscopic examination compared to the model group. It is worth noting that no ulcerative lesions were observed in the gastric tissues of rats receiving VKT upon microscopic examination. Our results indicated that Vien Khoi Tim capsules might possess a protective role against indomethacin-induced gastric ulcers. Additional research is needed to better understand the mechanism by which Vien Khoi Tim capsules exert their gastroprotective effect.

A recurrent ACTA1 amino acid change in mosaic form causes milder asymmetric myopathy

We describe three patients with asymmetric congenital myopathy without definite nemaline bodies and one patient with severe nemaline myopathy. In all four patients, the phenotype had been caused by pathogenic missense variants in ACTA1 leading to the same amino acid change, p.(Gly247Arg). The three patients with milder myopathy were mosaic for their variants. In contrast, in the severely affected patient, the missense variant was present in a de novo, constitutional form. The grade of mosaicism in the three mosaic patients ranged between 20 % and 40 %. We speculate that the milder clinical and histological manifestations of the same ACTA1 variant in the patients with mosaicism reflect the lower abundance of mutant actin in their muscle tissue. Similarly, the asymmetry of body growth and muscle weakness may be a consequence of the affected cells being unevenly distributed. The partial improvement in muscle strength with age in patients with mosaicism might be due to an increased proportion over time of nuclei carrying and expressing two normal alleles.