Thyroid storm is an endocrine emergency, and treatment must ensure primary goals, including reducing the production and release of thyroid hormones, mitigating the effects of thyroid hormones, increasing the elimination of thyroid hormones, treating systemic disturbances, and managing triggering factors. However, in a few cases where thyroid storm does not respond to initial treatment, therapeutic plasma exchange (TPE) should be considered. A 50-year-old male patient was admitted to the University Medical Center Ho Chi Minh City due to hypotonia and sensory disturbances gradually spreading from the lower extremities to the entire body. The patient was diagnosed with Guillain-Barré syndrome (GBS) and newly discovered hyperthyroidism. During the treatment course, the patient developed hospital-acquired pneumonia, acting as a trigger factor for a thyroid storm. Despite aggressive treatment for thyroid storm, the patient’s condition worsened, leading to the decision to perform TPE. The replacement fluid was a combination of fresh frozen plasma (FFP) and albumin 5%. Subsequently, the patient returned to a euthyroid state and was discharged. Combining FFP and albumin 5% in TPE advantages FFP’s high thyroid hormones-binding capacity and albumin’s cost-effectiveness, safety, and efficiency. This reduces the drawbacks associated with high volumes of FFP and offers a balanced and effective approach to managing thyroid storms. Moreover, the concurrent presence of GBS and thyroid storm is extremely rare. Through this case, we aim to discuss the role of TPE in the treatment of thyroid storms and the effectiveness of the combination of FFP and albumin 5% as the replacement fluid.

Neoadjuvant pyrotinib shows the potential to improve treatment response in human epidermal receptor 2 (HER2)-positive breast cancer patients, but relevant meta-analyses are scarce. This meta-analysis intended to explore the efficacy and safety of neoadjuvant pyrotinib for HER2-positive breast cancer patients. Studies comparing the efficacy and safety between HER2-positive breast cancer patients receiving pyrotinib-containing neoadjuvant treatment (pyrotinib group) and those receiving other neoadjuvant treatments (control group), were searched in EMBASE, Web of Science, Cochrane, PubMed, China National Knowledge Infrastructure, Wanfang, and SinoMed until December 2023. Six randomized controlled trials (RCTs) and 4 cohort studies were included. The pyrotinib group and control group contained 540 and 684 patients, respectively. Pathological complete response (pCR) was higher in the pyrotinib group than in the control group [relative risk (RR)=1.93; 95% confidence interval (CI) = 1.63-2.29; P < 0.001]. Similar results were discovered in subgroup analyses of RCTs (RR = 1.89; 95% CI = 1.49-2.40; P < 0.001) and cohort studies (RR = 1.98; 95% CI = 1.55-2.53; P < 0.001). The objective response rate (ORR) was also higher in the pyrotinib group than in the control group (RR = 1.14; 95% CI = 1.07-1.21; P < 0.001). Regarding adverse events, only the incidence of diarrhea was increased in the pyrotinib group versus the control group (RR = 1.97; 95% CI = 1.31-2.96; P = 0.001), while others were not different, including nausea and vomiting, leukopenia, thrombocytopenia, hand-foot syndrome, and alopecia (all P > 0.05). No publication bias existed, and sensitivity analysis suggested the satisfactory robustness of this meta-analysis. In conclusion, compared with other neoadjuvant treatments, pyrotinib-containing neoadjuvant treatment achieves a better treatment response with a good safety profile in HER2-positive breast cancer patients.

Retinal ischemia-reperfusion (I/R) is a pathological phenomenon that causes cellular destruction in several ocular disorders, so there is a need for novel possible neuroprotective drugs. Researchers have reported numerous neuroprotective effects of Germacrone (GM). Therefore, this study aimed to elucidate the underlying processes of GM that may contribute to glaucoma development. 40 healthy rats underwent retinal ischemia-reperfusion (I/R) damage. The animals were divided into control, I/R-induced, GM-1d, and GM-7d. After 7 days of I/R, mice were sacrificed and retinal tissue removed. An enzyme-linked immunosorbent assay (ELISA) was used to assess retinal Malondialdehyde (MDA) and 8-OHdG levels after oxidative injury. The Fluro-Gold (FG) labelling assay counted retinal ganglion cells (RGC) before and after labelling. DNA from retinal tissue RNA was amplified. Western blotting and real-time qRT-PCR were utilised to assess Bax, Casapses-3, Bcl-2, retinal NF-kB, and COX-2 expression. Retinal cell apoptotic mediator expression was measured by a TUNEL assay. Retinal I/R damage increases ganglion cell death. Long-term GM treatment (GM-7d) reduced NF-κB activation and raised COX-2 expression, which suggests antioxidant potential. TUNEL-positive apoptotic cells were reduced in long-term GM-treated rats. In GM-treated retinas, the Bax-Bcl-2 ratio was identical to the control group and significantly different from the I/R group. GM reduces I/R-induced retinal cell damage by inhibiting RG cell death. Seven days after GM therapy, histology showed retinal tissue loss. NF-κB signaling and intrinsic mitochondrial apoptosis are possible mechanisms that may be attenuated by GM and are attributed to a retinal protective effect.

Glioblastoma (GBM) is a malignant primary brain tumor and an essential contributor to morbidity and mortality globally. Arsenic trioxide (ATO) exerts specific roles in preventing tumor growth. This study investigated the role of ATO in GBM cell behaviors and stemness. The effects of ATO on the malignant behavior of GBM cells, tumor stemness, and epithelial-mesenchymal transition (EMT) factors in mouse tumor tissues were explored. Targets of ATO in GBM were predicted using multiple databases. Subsequently, the expression of retinoic acid-related orphan receptor beta (RORB), WNT-1, β-Catenin, and c-Myc expression were examined in GBM cells before and after ATO treatment.ATO inhibited the malignant behavior of GBM cells in vitro and slowed down the GBM growth in vivo by inhibiting the stemness. The inhibitory effect of ATO on GBM was achieved by promoting RORB levels and strengthening the antagonism to β-Catenin to inhibit Wnt signaling, thus inhibiting tumor growth. Collectively, ATO induced RORB levels in GBM cells and strengthened the antagonistic effect on β-Catenin, thus inhibiting WNT signaling and tumor growth.

In this study, we report two cases of siblings diagnosed with primary ciliary dyskinesia (PCD) sharing an identical genotype yet exhibiting distinct phenotypes. A 13-year-old girl with acute pneumonia was admitted to our hospital. Chest and sinus radiography revealed situs inversus and bilateral maxillary sinusitis. Chest computed tomography revealed bronchiectasis. Her 6-year-old brother with acute bronchitis was admitted and was diagnosed with bronchial asthma due to recurrent wheezing. Unlike his sister, he did not have situs inversus. Both patients had a chronic wet cough and were diagnosed with bronchial asthma by their family doctor. The mean PCD rule (PICADAR) scores were 9 and 7, respectively. Genetic analysis confirmed the presence of the same homozygous mutation (c.546C > A,pTyr182Ter) in DNAI2. To date, there have been four reports of the same pathogenic variants but different PCD phenotypes. Pathological variants of DNAI2 cause the loss of the outer dynein arm, the absence of which results in a lack of primary ciliary movement involved in the left-right axis formation during the embryonic period. A lack of functional cilia results in randomized visceral asymmetry; hence, the same pathogenic variant may exhibit different phenotypes. PCD is often overlooked and is sometimes managed as bronchial asthma, as in these siblings. In our case, the PICADAR score was useful in predicting the clinical diagnosis of PCD.