Hepatic myelopathy (HM) is a rare neurological complication in the end stage of many liver diseases and is characterized by bilateral spastic paraparesis without sensory and sphincter dysfunction. It occurs owing to metabolic disorders and central nervous system dysfunction associated with cirrhosis. Without timely and effective clinical intervention, the prognosis of these patients is devastating. Although liver transplantation (LT) is an effective treatment for HM, the prognosis of these patients remains unsatisfactory. Early recognition and diagnosis of this disease are essential for improving patient prognosis. Here, we report a case of hepatitis B virus-associated decompensated cirrhosis with HM. The patient recovered well after LT. We also summarize the clinical characteristics and post-transplant outcomes of 25 patients with HM treated by LT through 2023, including this case.

The clinical introduction of hepcidin25 (Hep25) has led to a more detailed understanding of its relationship with ferroportin (FP) and divalent metal transporter1 in primary iron overload syndromes (PIOSs). In 2012, we proposed a classification of PIOSs based on the Hep25/FP system, which consists of prehepatic aceruloplasminemia, hepatic hemochromatosis (HC), and posthepatic FP disease (FP-D). However, in consideration of accumulated evidence on PIOSs, we aimed to renew the classification.

We reviewed the 2012 classification and retrospectively renewed it according to new information on PIOSs.

Iron-loading anemia was included in PIOSs as a prehepatic form because of the newly discovered erythroferrone-induced suppression of Hep25, and the state of traditional FP-D was remodeled as the BIOIRON proposal. The key molecules responsible for prehepatic PIOSs are low transferrin saturation in aceruloplasminemia and increased erythroferrone production by erythroblasts in iron-loading anemia. Hepatic PIOSs comprise four genotypes of HC, in each of which the synthesis of Hep25 is inappropriately reduced in the liver. Hepatic Hep25 synthesis is adequate in posthepatic PIOSs; however, two mutant FP molecules may resist Hep25 differently, resulting in SLC40A1-HC and FP-D, respectively. PIOS phenotypes are diagnosed using laboratory tests, including circulating Hep25, followed by suitable treatments. Direct sequencing of the candidate genes may be outsourced to gene centers when needed. Laboratory kits for the prevalent mutations, such as C282Y, may be the first choice for a genetic analysis of HC in Caucasians.

The revised classification may be useful worldwide.

Three-dimensional power Doppler (3DPD) ultrasound has been used for assessing adnexal masses, and in this study, we aimed to perform a meta-analysis to evaluate its role in the differential diagnosis of adnexal masses.

A search for primary studies assessing the diagnostic performance of 3DPD in discriminating benign from malignant masses carried out between January 1990 and May 2023 was performed in Medline (PubMed), Scopus, and Web of Science databases with study quality evaluated using QUADAS-2.

We identified 404 citations. Ultimately, 18 studies comprising 2,975 women were included, and the mean prevalence of malignant lesions was 37%. In most cases, the quality of studies was moderate. Overall, pooled sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio of 3DPD vascular tree assessment for studies including any type of mass were 77% (95% confidence interval [CI] = 52%–91%), 80% (95% CI = 37%–97%), 3.9 (95% CI = 0.7–20.9), and 0.29 (95% CI = 0.10–0.81), respectively. Heterogeneity was high for both sensitivity and specificity. Pooled sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio of 3DPD vascular tree assessment for studies including only “complex” or “suspicious” adnexal masses were 90% (95% CI = 82%–94%), 88% (95% CI = 74%–95%), 7.3 (95% CI = 3.2–16.4), and 0.12 (95% CI = 0.06–0.22), respectively. Heterogeneity was moderate for both sensitivity and specificity. We could not perform quantitative synthesis for studies estimating 3D vascular indexes.

The diagnostic performance of 3DPD for discriminating benign from malignant adnexal masses is good, and there is great heterogeneity in diagnostic criteria when using this technique.

A mental disorder, also referred to as a psychiatric disorder or mental illness, is characterized by significant disturbances in an individual’s thinking, emotions, or behavior. In Ayurveda, herbal plants are used as alternative therapies for various ailments, including mental disorders. This review aims to provide a comprehensive overview of herbal medicines used in treating mental disorders in Sri Lanka. It relies on foundational books as primary sources to systematically identify and analyze the therapeutic potential of 24 traditional medicinal plants for treating mental disorders. Each plant was evaluated based on its scientific name, plant parts used, distribution in Sri Lanka, mechanisms of action, and identified phytochemicals. Furthermore, additional research was conducted using keywords such as mental disorders, herbal plants, plant distribution, phytochemicals, side effects, and mechanism of action through scientific databases. The phytochemicals present in these herbal plants possess antioxidant, anti-inflammatory, and neuroprotective properties, contributing to their potential antipsychotic activities. Trigonelline (from Abrus precatorius), bacosides (from Bacopa monnieri), asiaticoside and asiatic acid (from Centella asiatica), quercetin (from Ginkgo biloba), alliin and allicin (from Allium sativum), luteolin-7-O-glucoside (from Eclipta alba), and shogaol (from Zingiber officinale) demonstrate significant potential in modulating neurotransmitter levels, reducing oxidative stress, and alleviating symptoms associated with mental disorders such as depression, anxiety, and neurodegenerative diseases. The suggested therapeutic value of these identified herbal plants and their bioactive phytochemicals indicates the need for preserving and extensively investigating these remedies to establish their clinical effectiveness.

Chronic cholestasis due to heritable causes is usually diagnosed in childhood. However, many cases can present and survive into adulthood. The time course varies considerably depending on the underlying etiology. Laboratory data usually reveal elevated conjugated hyperbilirubinemia, alkaline phosphatase, and gamma-glutamyl transpeptidase. Patients may be asymptomatic; however, when present, the typical symptoms are pruritus, jaundice, fatigue, and alcoholic stools. The diagnostic methods and management required depend on the underlying etiology. The development of genome-wide associated studies has allowed the identification of specific genetic mutations related to the pathophysiology of cholestatic liver diseases. The aim of this review was to highlight the genetics, clinical pathophysiology, presentation, diagnosis, and treatment of heritable etiologies of chronic cholestatic liver disease.

Huaier (Trametes robiniophila Murr) is a traditional Chinese medicine with a clinical application history of over 1,000 years. Its chemical components mainly include polysaccharides, sterols, and alkaloids. Huaier has been shown to demonstrate potent antitumor effects in a variety of cancer types, including breast cancer, colorectal cancer, gastric cancer, liver cancer, lung cancer, and others. In recent years, multiple in-vitro experiments have confirmed the good antitumor effect of Huaier and its mechanism of action, such as inhibiting proliferation, inducing apoptosis and oxidative stress, interfering with cell cycle arrest, inhibiting tumor metastasis and angiogenesis, inducing autophagy, and regulating immune function. In addition, multiple in-vivo studies and clinical trials have demonstrated the multidimensional antitumor potential of Huaier, such as slowing tumor progression, reversing drug resistance, improving chemotherapy drug sensitivity, and extending the survival time of cancer patients. In this article, the extraction methods of Huaier and its properties for the treatment of many cancers are reviewed. Moreover, the current molecular mechanisms of Huaier are summarized, revealing that it has great potential as an anticancer drug and providing strong theoretical support for related research. Furthermore, this review also provides suggestions for further research on the anticancer effects of Huaier, hoping to offer fresh perspectives for researchers in the realm of anticancer medicine.

Herpetic Epithelial Keratitis is characterized by a corneal dendritic lesion, and prolonged or recurrent medication such as acyclovir, raises the possibility of resistant strains, necessitating the search for new therapies. An 84-year-old woman, phototype III, reported severe discomfort in the left eye. The presence of a dendritic ulcer was confirmed. Acyclovir therapy (oral—1.6 g/day and topical—seven days) was initiated and replaced by famciclovir (oral–1.5 g/day—seven days; topical acyclovir discontinued). Every three months, a new recurrence occurred. Famciclovir treatment (seven days) was subsequently supplemented with L-lysine (3 g—loading dose + 500 mg/day per 30 days) with L-arginine intake control. After amino acid supplementation, the clinical signs of the active lesion were reduced compared to previous treatment. Furthermore, a longer interval between recurrences was observed until they ultimately stopped. The patient is controlling L-arginine intake. When necessary, L-lysine supplementation is associated. Additional investigation is needed on the proposed supplementary therapy for Herpetic Epithelial Keratitis, which could help reduce side effects and resistance to antiviral drugs. However, as documented in this case report, amino acid supplementation can be recommended for controlling herpesvirus infection with no risk of adverse effects

Although multiple intricate and drawn-out in vivo investigations and complex in vitro assays are carried out as a part of the routine safety screening of drugs, medication failures arising out of safety-related issues continue to be an area of concern for pharmaceutical operations. Some of these failures may be explained by a lack of mathematical models to translate animal data into human data. Moreover, there may be differences in the sensitivity and drug disposition between humans and animals. Microphysiological systems may offer a way to more accurately represent these target tissues and a chance to better evaluate certain facets of human safety. As such, the ability of organs-on-chips to provide information at various development phases in drug discovery has sparked interest in recent years. This cutting-edge technology may aid in shedding light on the functioning of human organs and the pathophysiology of diseases. Also, they can be used to accurately predict the efficacy and safety of experimental medications in humans. Organs-on-chips know-how has been employed to successfully imitate specific nephron components including but not limited to the glomeruli, proximal as well as distal tubules, and collecting duct, all of which can be used in the testing of drugs for genetic kidney disorders. This review includes an overview of this technology along with some of its applications, challenges, and recommendations for the future.

A key element in the pathogenesis of metabolic syndrome (MetS) is the reprogramming of hypothalamic cells at the genetic level (in the prenatal phase), which leads to neuroinflammation. We hypothesize that alterations in the structure of hypothalamic neurons mediated by (epi)genetic alterations are directly related to impaired expression/production of neurotrophins and neurotransmitters that control the metabolism of substances in the brain and periphery, including brain-derived neurotrophic factor (BDNF). The aim of this review is to describe the molecular genetic and epigenetic role of BDNF in the development of MetS. Articles entered into the National Library of Medicine Medline database via the PubMed interface were used to create this review. We attempted to include as much literature as possible, including reviews, animal studies, cell culture studies, and clinical trials. Studies on BDNF point to its role in metabolic processes, including glucose, insulin, and cholesterol homeostasis. Evidence-based studies show that multiple genes in close proximity to BDNF are involved in the development of MetS. Studies aimed at analyzing BDNF in metabolic diseases using different biological samples will reveal clear pathophysiological links between processes in the brain and in the periphery.