Annals of clinical and laboratory science最新文献

A 46-year-old female presented with back pain associated with progressive bilateral lower extremity weakness and paresthesia. Imaging studies revealed a retroperitoneal mass with severe spinal compression. Histological sections showed blastoid cells with large nuclei, irregular membranes, fine chromatin, and prominent nucleoli. Immunohistochemical stains (IHC) showed neoplastic cells positive for B-cell markers. This patient was diagnosed with a high-grade B-cell lymphoma before transferred to our institution for further work-up. After review of the case, additional IHC was requested which revealed positivity for CD117 and myeloperoxidase (MPO). The overall morphological and immunophenotypical features were most compatible with myeloid sarcoma with aberrant expression of B-cell markers and this patient's diagnosis was amended. A literature review showed that 40-50% of myeloid sarcomas are misdiagnosed as lymphoma since they can frequently stain with B-cell or T-cell markers, which makes it challenging for an accurate diagnosis and sub-classification. We present this case to raise awareness of the potential diagnostic pitfalls.

Tuberculosis (TB) poses a significant public health challenge in India. According to the World Health Organization (WHO), India tops the list of 30 countries responsible for 87% of global TB cases in 2023. Recent data indicates that India's TB incidence rate was 195 cases per 100,000 population in 2023, accounting for approximately 26% of global TB cases. Global health organizations like the WHO and the Centers for Disease Control and Prevention (CDC) emphasize molecular techniques, such as Cartridge-Based Nucleic Acid Amplification Test (CB-NAAT), sequencing, and serological tests, to improve the accuracy and efficiency of TB diagnosis. The Government of India initiated the National Tuberculosis Elimination Program (NTEP), aiming for a TB-free India by 2025. Despite the efforts, practice gaps remain in diagnosis, treatment, and monitoring. Accelerated strategies focusing on early detection, management of latent TB, and control of drug resistance are critical. This review explores global guidelines, highlights implementation challenges, and suggests pathways for achieving effective TB control in India.

Objective: Myocardial injury is a prevalent complication of sepsis. This study aims to shed light on the role of Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) in regulating Fatty Acid Synthase (FASN) to identify the intrinsic molecular mechanisms of sepsis-induced myocardial injury.

Method: H9c2 cells were treated with Lipopolysaccharide (LPS) to model sepsis-induced cardiomyocyte injury and were subsequently divided into seven groups: Control, LPS, LPS+sh-NC, LPS+sh-ACSL4, LPS+sh-ACSL4+Erastin, LPS+sh-ACSL4+oe-NC, and LPS+sh-ACSL4+oe-FASN. Immunofluorescence staining and Western blot analysis were used to assess the expression levels of ACSL4, FASN, GPX4, and FTH1. Co-immunoprecipitation was conducted to investigate the interaction between ACSL4 and FASN. Additionally, levels of LDH, MDA, GSH, SOD, and iron were measured. We employed the CCK-8 assay and flow cytometry to determine cell viability and apoptosis rates.

Result: Compared with the control group, the LPS group showed decreased cell viability, increased apoptosis rate, elevated levels of LDH, MDA, and iron, reduced GSH and SOD levels, upregulated ACSL4 and FASN expression, and downregulated GPX4 and FTH1 expression. Treatment with sh-ACSL4 helped to ameliorate these changes. In the LPS+sh-ACSL4+Erastin group, cell viability declined further, apoptosis rate increased, and LDH, MDA, and iron levels were elevated, while GSH and SOD levels decreased, and GPX4 and FTH1 expression were reduced compared with the LPS+sh-ACSL4 group. Co-immunoprecipitation revealed an interaction between ACSL4 and FASN. Knockdown of ACSL4 combined with FASN overexpression attenuated the protective influence of ACSL4 knockdown on H9c2 cells.

Conclusion: ACSL4 may play an important role in LPS-induced cardiomyocyte injury by influencing the process of ferroptosis via FASN.

Objective: To explore the influence of abietic acid on the autophagy and apoptosis of cardiomyocytes in rats with acute myocardial infarction (AMI).

Methods: A rat model of AMI was built by ligation of the anterior descending branch of left coronary artery, and a model of hypoxic cardiomyocyte injury was constructed by treating cardiomyocytes with hypoxia. Western blot assay was used to detect the abundance of proteins related to autophagy and apoptosis, MTT assay was used to measure the viability of cardiomyocytes, and the expression level of miR-30a-5p was detected by qRT-PCR. The targeting relationship between miR-30a-5p and GRP78 was determined by double luciferase reporter gene experiment.

Results: After treatment with abietic acid (315mg/kg), the infarct area of AMI rats was noticeably debased, the intensity of cardiomyocyte autophagy was raised and the level of cardiomyocyte apoptosis was decreased. qRT-PCR results showed that abietic acid inhibited the expression of miR-30a-5p. Furthermore, the dual luciferase reporter gene assay demonstrated that miR-30a-5p targets GRP78. It was found that miR-30a-5p mimic could increase the expression of P62, decrease the LC3II/LC3I ratio, promote the expression of BAX, and reduce the expression of anti-apoptotic protein BCL2, while the effect of GRP78 on cardiomyocytes was opposite to that of miR-30a-5p. After the hypoxic myocardial cells were treated with 50 μM abietic acid, the standard of miR-30a-5p decreased and the abundance of GRP78 increased. After the hypoxic myocardial cells were treated with 50 μM abietic acid, the level of miR-30a-5p decreased and the abundance of GRP78 increased.

Conclusion: Abietic acid alleviates the hypoxic injury of cardiomyocytes by adjusting autophagy and apoptosis mediated by miR-30a-5p/GRP78 axis.

Objective: To understand the influence of MIR-451 on LKB1-AMPK signal pathway and oxidative stress index in lung cancer mice.

Methods: 40 rats were divided into four groups: ZC group (no lung cancer model), model group (lung cancer model), intervention group (rats with MiR-451 agomir injected), and NC group (rats with MiR-451 agomir control injected), 10 mice/group. The levels of MDA (malondialdehyde) and SOD (superoxide dismutase) in the four groups were detected, as well as the overall weights of the lungs and spleens. Lung tissue pathological changes were assessed by HE and LKB1-AMPK protein level and mRNA by Western blot and PCR.

Results: Compared to ZC group, the MDA levels in model and NC group were higher (p<0.05). In comparison with model and NC groups, the MDA level in intervention group was lower (p<0.05), while SOD was inversely associated with MDA levels. The lung and spleen indexes were similar in the NC and model groups (p>0.05). The lung index was lower and spleen index was higher in intervention group than in the other two groups (p<0.05). LKB1 and AMPK protein levels in model and NC groups were significantly elevated over the ZC group (P<0.05), and the LKB1 and AMPK protein levels of intervention group were the highest (P<0.05); LKB1 and AMPK mRNA levels of model and NC group were minor than ZC and intervention group (P<0.05).

Conclusion: MiR-451 agonist shows a favorable response in a lung cancer model, reducing MDA levels and increasing SOD levels and improving lung weight as well as increasing LKB1-AMPK protein and mRNA expression.

Objective: To investigate the therapeutic effects of Cornus officinalis iridoid glycosides (CIG) on rats with chronic renal failure (CRF).

Methods: CRF was induced in adult male Sprague Dawley rats by nephrectomy. The rats were randomly divided into six groups: sham, sham+high-dose CIG (120 mg/kg/d for 14 days), CRF, CRF+low-dose CIG (60 mg/kg/d for 14 days), CRF+high-dose CIG, and CRF+high-dose CIG+ML385 (an inhibitor of nuclear factor erythroid 2-related factor 2 (Nrf2), single administration at 30 mg/kg). The pathohistological changes in renal tissues were evaluated with histological staining. The biomarker levels of renal function, oxidative stress, inflammation, and apoptosis, as well as Nrf2 expression in renal tissues were determined.

Results: The rats in the sham and sham+high-dose CIG groups showed normal renal tissues. The rats in the CRF group displayed severe renal tissue damage/fibrosis and elevated biomarkers of renal dysfunction, which were accompanied by decreased nuclear and cytoplasmic Nrf2 expression and elevated levels of oxidative stress, inflammatory, and apoptotic markers in renal tissues. CIG treatment of CRF rats attenuated renal tissue damage and fibrosis, with the high-dose drug showing more significant improvements. The high-dose CIG also restored renal function in CRF rats, upregulated Nrf2, and downregulated oxidative stress, inflammatory, and apoptotic markers in renal tissues. These effects of high-dose CIG on CRF rats were reversed by ML385.

Conclusions: CIG activates the Nrf2-antioxidant pathway to ameliorate oxidative and inflammatory renal tissue damage and restore renal function in CRF rats.

Objective: Urinary cytology is a key diagnostic tool for evaluating suspected urinary tract carcinoma, primarily high-grade urothelial carcinoma. The Paris System for Reporting Urinary Cytology (TPS), introduced in 2016, aimed to standardize reporting, though challenges with subjectivity and variability in diagnosing Atypical Urothelial Cells (AUCs) persist.

Methods: This retrospective study explored the correlation between cytomorphological features in "atypical" diagnosis and UroVysion fluorescence in-situ hybridization (U-FISH) results. We assessed 19 cytomorphologic parameters in 121 cases. Histologic diagnosis, clinical findings, and patient history were also documented.

Results: Of 121 cases, 38 (31.4%) tested U-FISH positive. The sensitivity and specificity of U-FISH in detecting malignancy were 93.5% and 91.1%, respectively. Five cytologic parameters-high atypical cellularity, nuclear/cytoplasmic ratio ≥0.7, nuclear enlargement (≥2.5 times), multinucleation, and mitosis-were significantly associated with U-FISH positivity. No association was found between TPS AUC criteria and U-FISH positivity. The majority of combinations of these key parameters exhibited high PPVs (>65.0%), suggesting their potential for classifying cases without U-FISH.

Conclusions: Cases exhibiting combinations of these five parameters or any four including mitosis demonstrated a 100% positive predictive value (PPV). However, subsets of cases with certain parameter combinations showed moderate PPVs, indicating the potential utility of reflex U-FISH testing.

Objective: The aim of the present study was to determine the effects of selenium-methylselenocysteine (MSC) on the viability, migration, and glycolysis of human ATC cell lines 8305 and BHT101 in vitro.

Methods: Cells were treated with MSC and viability was determined using the Cell Counting Kit 8 assay. The migratory ability of cells was detected using a Transwell migration assay, and the expression levels of proteins involved in the ERK1/2, JNK, and p38 signaling pathways were measured by western blotting. Glycolysis was investigated by determining glucose consumption, lactate production, and protein levels of key glycolytic enzymes (glucose transporter 1, hexokinase 2, and lactate dehydrogenase A).

Results: MSC inhibited the viability, migration, and glycolysis of ATC cells. Phosphorylated (p)-ERK1/2 expression decreased with increasing MSC concentration; however, p-JNK and p-p38 levels were unaffected in cell lines 8305C and BHT101. Epidermal growth factor induced activation of ERK1/2 and impaired the inhibitory effect of MSC on ATC cell viability, migration, and glycolysis.

Conclusions: These findings indicated that MSC inhibited the viability, migration, and glycolysis of ATC cells via the ERK1/2 signaling pathway, suggesting that MSC may represent a novel therapeutic agent for ATC.