Accurate identification of invasive fungal pathogens is crucial for appropriate antifungal therapy. The Department of Clinical Laboratory at Indus Hospital & Health Network, Karachi, Pakistan, reported two cases of invasive fungal infections between 1st January and 31st March 2024 in which conventional identification methods and automated systems produced discordant results, highlighting critical diagnostic challenges.

Two invasive yeast isolates initially showing budding yeast cells without pseudohyphae on Gram stain were subjected to conventional identification using cornmeal-Tween 80 agar, chrome agar, and BiGGY agar, followed by automated identification using the VITEK 2 ID-YST system and confirmatory API 20C AUX testing. Both isolates demonstrated typical soft, wrinkled, cream-colored colonies on Sabouraud dextrose agar, which on chrome agar appeared as dry, blue colonies and on BiGGY agar as dry, brown colonies. Characteristic arthroconidia and blastoconidia formation on cornmeal-Tween 80 agar were observed, consistent with Trichosporon species. However, the VITEK 2 ID-YST system identified both isolates as Cryptococcus laurentii with good confidence levels. India ink staining was negative for both isolates. Confirmatory API 20C AUX testing correctly identified both isolates as Trichosporon asahii (identification profile 3740734).

This discordance between automated and conventional methods underscores the continued importance of conventional identification techniques and highlights potential limitations of automated systems for certain uncommon yeasts. Laboratories should maintain proficiency in conventional methods and consider confirmatory testing when automated results conflict with morphological findings. The clinical implications of misidentification include inappropriate antifungal selection, given the different susceptibility patterns between these species.

Human immunodeficiency virus (HIV)/hepatitis C virus (HCV) coinfection leads to severe systemic inflammation, increasing non-AIDS morbidity and mortality risk. CD39 ectoenzyme on T-cells, which catalyzes the conversion of pro-inflammatory purines to immunosuppressive adenosine, plays an important role in inflammation control. The role of CD39+ T-cells in systemic inflammation during HIV/HCV coinfection under antiretroviral therapy (ART) remains unexplored. This study aimed to identify specific patterns of CD39 expression on T-cells in ART-treated HIV/HCV coinfected patients and assess their relationship with systemic inflammation.

We conducted a case-control study that enrolled 41 HIV/HCV coinfected patients on stable ART (cases) and 23 healthy controls. CD39 expression on blood CD4+ and CD8+ T-cells, including CD45RA+ and CD45RA– subsets, was quantified using flow cytometry. Cytokines were assessed using multiplex and enzyme-linked immunosorbent assays.

A significant proportion of CD4+ T-cells expressed CD39 in both groups (cases – 24.0%; controls – 16.1%). That was not true for CD8+ T-cells (cases – 3.2%; controls – 2.8%). CD39 expression was higher on CD45RA+ than CD45RA– CD4+ T-cells (cases – 39.4% vs. 19.0%; controls – 24.6% vs. 9.2%). HIV/HCV coinfected patients exhibited a significantly increased proportion of CD39+ CD4+ T-cells compared to uninfected controls (P < 0.01). A negative correlation was observed between the percentage of CD39+ CD4+ CD45RA– T-cells and levels of pro-inflammatory chemokines monocyte chemoattractant protein 1 (R = –0.392; P < 0.01) and eotaxin (R = –0.325; P < 0.05).

The data suggest a compensatory expansion of cells with regulatory properties that is ultimately insufficient to control systemic immune activation.

Phenylethanoid glycosides (PhGs) are water-soluble natural compounds widely distributed in the plant kingdom, attracting significant attention from medicinal chemists due to their promising potential in pharmaceutical applications. PhGs exhibit a broad range of activities, including neuroprotective, hepatoprotective, anti-inflammatory, antioxidant, and immunomodulatory effects. This review aims to update the hepatoprotective effects of total PhG extracts and individual PhG compounds, as well as the underlying mechanisms. Additionally, we describe the structural characteristics, representative PhG compounds, and their structure–activity relationships. In brief, total PhG extracts can exert synergistic protection by reducing serum alanine aminotransferase/aspartate aminotransferase levels, suppressing oxidative stress, and attenuating inflammatory responses. Representative PhGs, including acteoside (verbascoside), echinacoside, forsythoside A (also known as forsythiaside A), and cistanoside A, protect against liver injury through modulation of the Nrf2/HO-1, NF-κB, MAPK, and TGF-β/Smad pathways, thereby regulating oxidative stress, inflammation, apoptosis, fibrosis, and lipid metabolism. Structurally, PhGs consist of a phenylethyl alcohol core, cinnamoyl residues, and glycosyl moieties. Structure–activity relationship analyses indicate that caffeoyl substitution, multiple phenolic hydroxyl groups, and optimal glycosylation patterns are key determinants of hepatoprotective efficacy.

Pancreatic cystic neoplasms (PCNs) are increasingly detected in clinical practice, yet substantial variability exists in imaging interpretation and reporting, which may affect clinical decision-making. This guideline was developed to standardize diagnostic imaging evaluation and reporting for PCNs. A multidisciplinary expert panel conducted literature search and critical appraisal of domestic and international evidence, identified key clinical questions, and formulated recommendations using the Grading of Recommendations Assessment, Development and Evaluation framework. A modified Delphi consensus process and external review were performed to ensure the robustness of the recommendations. A total of 21 key questions were addressed, covering essential aspects of imaging evaluation and reporting for PCNs, including the preferred imaging modality for suspected lesions; standardized measurement of cyst size and mural nodules and their clinical significance; definitions of cyst wall and septal thickening; optimal imaging approaches for assessing the relationship between cystic lesions and the main pancreatic duct; measurement and evaluation of main pancreatic duct diameter and dilation; imaging-based classification of intraductal papillary mucinous neoplasms and serous cystic neoplasms; assessment of ductal obstruction, calcification, hemorrhage, and pancreatitis-related changes; criteria for suspicious lymph nodes; differentiation of PCNs from pancreatic pseudocysts or retention cysts; and recommended imaging modalities and follow-up intervals. This guideline provides a structured and evidence-based framework for imaging evaluation and reporting of PCNs, which may improve the consistency and clarity of imaging reports and support clinical decision-making.

Glioblastoma remains a highly challenging malignancy with a pronounced tendency for recurrence. The hypoxic microenvironment is a key contributor to its therapy resistance. Hyperbaric oxygen therapy (HBOT), which elevates tissue oxygen pressure and reverses hypoxia, exhibits a “dual effect” in glioblastoma management. This review aims to evaluate the therapeutic potential of HBOT in glioblastoma by examining its multifaceted effects on tumor biology and treatment response. On one hand, it enhances radiosensitivity through reactive oxygen species generation, increases chemotherapy efficacy by augmenting cytotoxicity and improving vascular perfusion, and remodels the tumor microenvironment via vessel normalization, edema reduction, and immune cell modulation. Furthermore, HBOT attenuates cancer stem cell properties by downregulating stemness markers and inhibiting self-renewal capacity. On the other hand, HBOT may also promote tumor progression: oxidative stress can induce genomic instability, while concomitant activation of HIF-, NF-κB-, and VEGF-mediated pro-survival pathways may facilitate malignant cell adaptation and proliferation. Given these opposing considerations, the clinical application of HBOT in glioblastoma management remains exploratory. In conclusion, future research should focus on optimizing HBOT protocols. In addition, exploring combination with other therapeutic approaches is equally important. These efforts are essential for the safe and effective integration of HBOT into comprehensive treatment strategies for glioblastoma.

Due to the lack of specific Western medicine therapies for post-coronavirus disease 2019 (COVID-19) syndrome in clinical practice, this study aimed to investigate the efficacy of traditional Chinese medicine (TCM) for post-COVID-19 syndrome using a cohort study design and to explore its clinical value in alleviating patients’ symptoms and improving clinical outcomes.

In this cohort study, patients were divided into two groups according to clinical treatment. The control group received conventional Western medicine, and the treatment group received additional TCM syndrome differentiation–based treatment. Propensity score matching methods were used to reduce selection bias by equating groups based on observed covariates. Clinical data, including TCM symptom scores, the Short Form 36 Health Survey, clinical efficacy, and adverse events at Day 7, were collected. The primary outcome was the efficacy rate, defined by improvement at Day 7 compared with the Day 0 score. Data were processed and analyzed using SPSS 23.0 and R 4.5.0 software.

A total of 434 patients were enrolled in the cohort, including 306 patients in the control group and 128 in the treatment group. After 1:1 matching, 94 matched pairs were analyzed. For the primary outcome, the effective rate in the treatment group was higher than that in the control group (30.8% vs. 17.2%; odds ratio (OR) = 2.17, 95% confidence interval (CI): 1.09–4.35, P = 0.003). After seven days of treatment, the TCM syndrome score improved more in the treatment group than in the control group (median difference (MD) = 2.00, 95% CI: 0.50–3.50, P = 0.009). Subgroup analyses showed generally favorable efficacy in the treatment group across subgroups, though not all reached statistical significance.

TCM syndrome differentiation–based therapy effectively relieves clinical symptoms in patients with post-COVID-19 syndrome.

Metabolic dysfunction–associated steatotic liver disease (MASLD), defined by the American Association for the Study of Liver Diseases as hepatic steatosis with at least one cardiometabolic risk factor, affects approximately 30–40% of adults worldwide. This condition may progress to fibrosis, cirrhosis, and hepatocellular carcinoma. The rising prevalence, alongside obesity and type 2 diabetes, underscores the need for early risk stratification and integrated therapeutic strategies. Circadian homeostasis, orchestrated by the suprachiasmatic nucleus and core clock gene feedback loops, synchronizes hepatic metabolic pathways with environmental light–dark cycles. The objective of this review is to evaluate the role of circadian disruption and metabolic dysfunction in the development of hepatic steatosis, as well as to assess current and potential treatment modalities for both disorders. Circadian disruption through shift work, artificial light at night, sleep restriction, and chrono-nutritional misalignment destabilizes hepatic clocks, promoting insulin resistance, dyslipidemia, inflammation, and steatosis. Experimental models demonstrate that clock gene dysfunction alone can induce steatohepatitis, while progressive MASLD further impairs central circadian regulation, establishing a self-reinforcing chrono-metabolic cycle. Pharmacologic therapies, including glucagon-like peptide-1 receptor agonists and thyroid hormone receptor-β agonists, improve histologic endpoints and fibrosis regression, although heterogeneity among clinical trials precludes direct comparison. Recent evidence characterizing MASLD as a predominantly nocturnal metabolic disorder further highlights persistent nighttime insulin dysregulation despite weight loss, emphasizing the potential role of circadian-targeted interventions such as melatonin. In conclusion, the peripheral circadian clock is intricately linked with MASLD pathogenesis, and metabolic dysfunction, in turn, disrupts circadian pathways. Several pharmacologic therapies offer potential for the treatment of MASLD and circadian dysfunction.

Pancreatic fibrosis, a major pathological feature of chronic pancreatitis, is primarily driven by the abnormal activation of pancreatic stellate cells (PSCs) and excessive deposition of extracellular matrix. Traditional Chinese medicine (TCM) offers a holistic and synergistic approach to preventing and treating pancreatic fibrosis through multi-target regulation of PSC activation. This review systematically elucidates the mechanisms by which TCM—encompassing both bioactive monomers and compound formulations—modulates key signaling pathways involved in PSC activation, including the mitogen-activated protein kinase, transforming growth factor-β/Smad, platelet-derived growth factor, nuclear factor kappa B, and Wingless/β-catenin pathways. By simultaneously targeting these interconnected signaling networks, TCM strategies effectively inhibit PSC activation, attenuate inflammatory responses, and reduce extracellular matrix deposition. In contrast to single-target pharmacological inhibitors, TCM embodies a “multi-component, multi-pathway” therapeutic paradigm that aligns with the complex pathophysiology of pancreatic fibrosis. This review also draws comparative insights from liver fibrosis, highlighting conserved pathways and organ-specific regulatory contexts. Ultimately, TCM represents a promising integrative avenue for the prevention and treatment of pancreatic fibrosis, supported by growing preclinical evidence and aligned with the principles of holistic intervention.

Hashimoto’s thyroiditis (HT), an autoimmune disease with a prevalence 2–7 times higher in women than in men, is associated with daytime sleepiness. The present study aimed to test the hypothesis that thyroid function is associated with chronotype and daytime sleepiness in women with HT.

This retrospective cross-sectional study included women with confirmed HT. Demographic, clinical and laboratory data were collected. The reduced Morningness-Eveningness Questionnaire (rMEQ) and the Epworth Sleepiness Scale (ESS) were used to assess chronotype and daytime sleepiness, respectively. Based on rMEQ, women were categorized as having a morning (≥18), intermediate (12–17) or evening (≤11) chronotype. Based on ESS, women were categorized as having normal or increased daytime sleepiness.

Overall, 106 women, aged 43 ± 12 years, were included. Most had normal daytime sleepiness (68.9%), and the majority had an intermediate chronotype (61.3%), while only one had a morning chronotype (0.9%). Age was significantly associated with chronotype (P = 0.026). There was a significant association between chronotype and thyroglobulin antibodies (TgAb, P = 0.012). Free triiodothyronine (fT3) levels were significantly higher in women with an evening chronotype than in those with an intermediate chronotype (P = 0.045; OR = 0.500; 95% CI 0.25–0.98). Daytime sleepiness was significantly associated with TgAb (P = 0.016) and thyroid-stimulating hormone (TSH, P = 0.040). TgAb levels were significantly higher in women with increased daytime sleepiness (P = 0.049, OR = 1.003, 95% CI 1.00–1.01) than in those with normal daytime sleepiness.

Approximately one-third of women have an evening chronotype, and approximately one-third had increased daytime sleepiness. TgAb, fT3, and TSH are associated with daytime sleepiness or chronotype in women with HT. Further investigation is required for the underlying mechanisms.