Assessing the effect of transcranial magnetic stimulation on peak cough flow in patients with supratentorial cerebral infarction: A retrospective cohort studyYoo, Seung Don; Park, Eo Jin
doi: 10.1097/md.0000000000033689pmid: 37115059
Respiratory dysfunction following supratentorial cerebral infarction leads to pneumonia and is a major cause of mortality. Decreased voluntary cough function impairs the ability to clear mucus or secretions from the airways and increases the risk of aspiration pneumonia. Peak cough flow (PCF) is one of the objective tools for evaluating voluntary cough function. Repetitive transcranial magnetic stimulation (rTMS) could be applied to the respiratory motor cortex to improve respiratory function. Little is known about the effect of rTMS on PCF in patients with supratentorial cerebral infarction during the subacute period. This study aimed to determine whether rTMS treatment could improve PCF in patients with supratentorial cerebral infarction. We retrospectively recruited patients with subacute supratentorial cerebral infarction who underwent a PCF test. The rTMS group received a combination of rTMS treatment for 2 weeks and conventional rehabilitation for 4 weeks. However, the control group underwent only conventional rehabilitation for 4 weeks. PCF tests were performed before and after treatment and the results were compared between the 2 groups. In total, 145 patients with supratentorial cerebral infarctions were recruited. The PCF parameters before and after treatment increased in both the rTMS and control groups. However, the rTMS group showed a greater increase in PCF values compared with the control group. In patients with supratentorial cerebral infarction, the combination of conventional rehabilitation and rTMS in the subacute period may be helpful in improving voluntary cough function compared with conventional rehabilitation alone.
Wellens syndrome during chemotherapy for cholangiocarcinoma: A case report of cardiovascular toxicity associated with gemcitabine-containing regimenLiang, Xufei; Geng, Xuhong; Gong, Xiaohong; Yin, Xi; Chen, Yongzhen
doi: 10.1097/md.0000000000033599pmid: 37115080
Rationale:
Wellens syndrome is a comprehensive electrocardiographic (ECG) diagnosis that combines medical history with characteristic ECG changes. These changes, characterized by biphasic T-wave inversions or symmetric and deep T-wave inversions in the anterior precordial leads, often indicate that the left anterior descending coronary artery is at a high risk of severe stenosis. Chemotherapy-related cardiovascular toxicity refers to damage to the cardiovascular system caused by chemotherapeutic drugs, which is unpredictable and may occur during or after chemotherapy.
Patient concerns:
In this case report, a 41-year-old male patient with cholangiocarcinoma received sequential adjuvant chemotherapy with gemcitabine/nanoparticle albumin–bound paclitaxel and gemcitabine/cisplatin. This patient presented with recurrent brief chest pain episodes after the third dose of gemcitabine/cisplatin, and the characteristic T-wave morphological changes were captured in routine ECG monitoring prior to the 6th dose.
Diagnoses:
Acute coronary syndrome due to chemotherapy-related cardiovascular toxicity was diagnosed on the basis of characteristic ECG changes.
Interventions:
The patient underwent coronary angiography, which revealed diffuse stenosis of up to 95% in the middle segment of the left anterior descending coronary artery. Stents were implanted in the stenotic segment for vascular reconstruction.
Outcomes:
The patient’s chest pain was completely resolved, and electrocardiography returned to normal.
Lessons:
Cardiovascular toxicity during chemotherapy in patients with cancer may be life threatening. This rare case highlights the importance of identifying the characteristic ECG pattern of the Wellens syndrome by monitoring electrocardiography during chemotherapy. Immediate and accurate identification of the morphological ECG features of Wellens syndrome with a slight elevation of the ST-segment is related to patient prognosis.
A bibliometric analysis of obstructive sleep apnea and anesthesiaÖner, Özlem; Ecevit, Mustafa Cenk; Gökmen, Ali Necati
doi: 10.1097/md.0000000000032993pmid: 37115083
To conduct a bibliographic analysis of obstructive sleep apnea (OSA) which has reached epidemic proportions and is a frequent, unknown, and important cause of perioperative morbidity and mortality, by examining the internationally most cited articles. For OSA, the most cited articles in the field of anesthesiology and reanimation, appropriate access terms were compiled and combined, and related publications were searched using the Thompson Reuters Web of Science Citation Indexing search engine. A total of 79 journal publications were found on OSA and anesthesia, with an average of 14.86 citations per article. The most cited publication was the “Society for Ambulatory Anesthesia Consensus Statement on Preoperative Selection of Adult Patients with Obstructive Sleep Apnea Scheduled for Ambulatory Surgery” published in the journal Anesthesia and Analgesia and was conducted by Joshi et al. It was found that 38 of the 79 studies reached as a result of the search were articles, and the average number of citations was 21.13. The Hirsch index of these articles, which were cited 803 times in total, was 15. A total of 31 articles (81.57%) were cited at least once, while the remaining 7 articles (18.43%) were not cited at all. The majority of the articles obtained are from the research fields of anesthesiology (n = 20; 52.63%), followed by otorhinolaryngology (n = 5; 13.15%), pediatrics (n = 5; 13.15%), respiratory system (n = 5; 13.15%), internal medicine (n = 4; 10.52%), and the rest were in various fields. Publications on “Obstructive Sleep Apnea” and “Anesthesia” have increased rapidly in the last decade. Anesthesia management and airway safety, patient management, including pain control in the postoperative period, and noninvasive mechanical ventilation treatment methods, such as continuous positive airway pressure, are hot topics.
CT findings of glycogen storage disease I complicated with pancreatitis: A case reportChen, Shuo; Chen, Feng; Cheng, Fei; Xu, Xiao
doi: 10.1097/md.0000000000033668pmid: 37115055
Rationale:
The incidence of glycogen storage disease type I (GSD I) in the overall population is 1/100,000.[1] Hyperlipidemia in patients with GSD I can induce pancreatitis. Three cases of GSD I complicated with pancreatitis have been reported.[2] Here, the computed tomography (CT) features of GSD I complicated with pancreatitis are reported for the first time
Patient concerns:
A 22-year-old female presents with growth retardation for 20 years and recurrent epigastric pain for 3 years. No abnormality in physical examination. Laboratory examination: GPT 81 U/L, GOT 111 U/L, DBIL 1.7 umol/L, TBIL 0.7 umol/L, Albumen 41.4 g/L, blood ammonia 54 umol/L, fasting blood glucose 3.02 mmol/L, G6PD 1829 U/L, lactic acid 7.9 mmol/L, triglyceride 18.79 mmol/L, TCH 9.46 mmol/L, uric acid 510 umol/L, urinary protein +++ (3.0) g/L.
Diagnosis:
The CT findings of the upper abdomen show that the liver is obviously enlarged, and the density of the liver is obviously uneven on plain scan. Unclear boundaries and increased blood vessels of the pancreas are found, especially in the head of the pancreas. The patient is diagnosed with GSD I complicated with pancreatitis.
Interventions:
The patient undergoes split liver transplantation and splenectomy under general anesthesia in our hospital.
Outcomes:
Upper abdominal CT is reexamined half a month and 2 and a half months after the operation. It is found that the transplanted liver is not enlarged and the density is not abnormal. The pancreas shrinks, its boundary is clear, and its blood vessels decrease, especially in the head of the pancreas
Lessons:
The density of the liver depends on the relative amount of glycogen and fat, which can be increased, normal, or decreased. Hyperlipidemia in patients with GSD I can induce pancreatitis.
Effects of continuous positive air pressure on intraocular pressure in patients with obstructive sleep apnea during the split-night study: An open-label randomized controlled trialFukutome, Takero; Kuze, Manami
doi: 10.1097/md.0000000000033566pmid: 37115064
Background:
Intraocular pressure (IOP) is known to increase at midnight, when continuous positive airway pressure (CPAP) is initiated in split-night CPAP titration (SN-CPAP titration), in patients with obstructive sleep apnea (OSA); therefore, possible excessive increase in the IOP should be investigated. However, related studies on this topic are scarce. OSA causes increases and decreases in the IOP; however, its fluctuation during sleep remains unclear. Therefore, we determined the timing of these fluctuations in the IOP during sleep at night.
Methods:
This study included 25 patients with OSA. A 7-hour period of night sleep was divided into first (Sleep-1) and second halves (Sleep-2). Patients were randomly divided into the SN (natural breathing during Sleep-1, CPAP applied during Sleep-2) and C (without CPAP) groups. IOP was measured using the iCare Pro before Sleep-1 and after Sleep-1 and Sleep-2. The main hypothesis was that IOP would be significantly higher in the SN group than in the C group. The sub-hypothesis was that the effects of OSA on IOP are manifested at different times. The correlation is shown as Pearson’s r for normally distributed data or Spearman’s rho for non-normally distributed data. The difference between the SN and C groups in the time course of IOP during the night’s sleep was analyzed using repeated-measures analysis of variance. A P value of <.05 was considered significant.
Results:
No significant difference was found in IOP between the groups, but the SN group showed a significantly increased IOP during Sleep-2 (post hoc Bonferroni test). The apnea–hypopnea index inversely correlated with IOP changes in Sleep-1 and positively correlated with those in Sleep-2.
Conclusion:
This study does not support our main hypothesis that SN-CPAP titration promotes the effect of CPAP in increasing IOP. However, an expected range of the effect of increased CPAP on IOP has also been suggested. IOP-lowering and IOP-raising effects were predominant in the first and second halves of sleep in OSA, thereby providing a new perspective on measured IOP and supporting the subhypothesis.
The association of hepcidin, reticulocyte hemoglobin equivalent and anemia-related indicators on anemia in chronic kidney diseaseGao, Zhaoli; Hu, Yingying; Gao, Yanxia; Ma, Xiaotian; Hu, Zhao
doi: 10.1097/md.0000000000033558pmid: 37115087
Hepcidin is an essential regulator of iron homeostasis in chronic kidney disease (CKD) anemia, reticulocyte hemoglobin equivalent (RET-He) can be used to evaluate the availability of iron for erythropoiesis. Previous research has found that hepcidin indirectly regulates RET-He. This study aimed to investigate the association of hepcidin, RET-He and anemia-related indicators on anemia in chronic kidney disease. A total of 230 individuals were recruited, including 40 CKD3-4 patients, 70 CKD5 patients without renal replacement therapy, 50 peritoneal dialysis patients, and 70 hemodialysis patients. The serum levels of hemoglobin (Hb), reticulocyte, RET-He, serum iron, serum creatinine, serum ferritin, total iron binding capacity, hepcidin-25, high sensitivity C-reactive protein, transferrin, erythropoietin, intrinsic factor antibody, soluble transferrin receptor and interleukins-6 (IL-6) were measured. Hepcidin-25 was positively associated with IL-6, and negatively with total iron binding capacity, intrinsic factor antibody, and transferrin. Reticulocyte Hb equivalent was associated positively with Hb, serum ferritin, serum iron, transferrin saturation, and negatively with serum creatinine, reticulocyte, IL-6, STfR. Hepcidin-25 was not associated with RET-He, while IL-6 was independently associated with hepcidin-25 and RET-He, suggesting that hepcidin has no effffect on the iron dynamics of reticulocytes in CKD, may be related to IL-6, indicate a likelihood of a threshold for stimulation of hepcidin-25 expression by IL-6 in order to indirectly regulates RET-He.
Association study of selenium-related gene polymorphisms with geriatric depression in ChinaLiu, Yu; Wang, Liqun; Wang, Zhizhong; He, Shulan
doi: 10.1097/md.0000000000033594pmid: 37115082
Depression is a common mental health problem in older adults, but its cause remains unclear. Selenium is an essential micronutrient and a powerful antioxidant in the brain and nervous system. Several recent studies have reported a relationship between selenium levels and depression. This study aimed to investigate the relationship between 4 genes co-associated with selenium and geriatric depression. 1486 participants were included in this study from 5 communities in Ningxia Hui Autonomous Region during 2013 to 2016 in a health examination program for urban and rural residents. Polymorphisms of 4 selenium-related genes were analyzed in 1266 healthy volunteers and 220 patients with depression. The genotyping of rs2830072, rs2030324, rs6265, rs11136000, rs7982, rs10510412, rs1801282, rs1151999, rs17793951, rs709149, rs709154, and rs4135263 were performed by Matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS) technology. The analysis of selenium-related genes showed that there were significant differences between depression and controls for allele and genotype frequencies of peroxisome proliferator activated receptor gamma (PPARG) rs10510412, rs709149, and rs709154 (all P < .05). In this study, when adjusting for age, sex, marital status, education, and alcohol consumption, results showed that rs709149 and rs709154 were still significantly correlated with geriatric depression in the codominant, dominant, overdominant, and log-additive models. Logistic regression analysis showed that rs709149 AG or GG gene carriers were 1.630 and 1.746 times more susceptible to depression than AA gene carriers (95% CI = 1.042–2.549; 1.207–2.526). The results of this study suggest that the rs709149 polymorphism of the selenium-related gene PPARG is a genetic risk factor for depression in older adults.
Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A reviewNiu, Jing; Liu, Yanli; Wang, Junjun; Wang, Hui; Zhao, Ying; Zhang, Min
doi: 10.1097/md.0000000000033651pmid: 37115081
The degeneration of articular cartilage tissue is the most common cause of articular cartilage diseases such as osteoarthritis. There are limitations in chondrocyte self-renewal and conventional treatments. During cartilage regeneration and repair, growth factors are typically used to induce cartilage differentiation in stem cells. The role of thrombospondin-2 in cartilage formation has received much attention in recent years. This paper reviews the role of thrombospondin-2 in cartilage regeneration and the important role it plays in protecting cartilage from damage caused by inflammation or trauma and in the regenerative repair of cartilage by binding to different receptors and activating different intracellular signaling pathways. These studies provide new ideas for cartilage repair in clinical settings.
Identification of LncRNA-miRNA-mRNA ceRNA network in hypoxia-induced HTR-8/SVneo cells for preeclampsiaLiu, Zhenzhen; Liu, Haiyan; Wang, Chengjie; Pei, Jiangnan; Chu, Nan; Peng, Ting; Li, Xiaotian; Gu, Weirong; Tang, Yao
doi: 10.1097/md.0000000000033649pmid: 37115060
Preeclampsia (PE) is a common pregnancy complication, and placental hypoxia is one of its causes. We aimed to identify the transcriptional profile and construct a long non-coding RNAs (lncRNA)-centered competing endogenous RNAs (ceRNA) network in hypoxia-induced HTR8/SVneo cells. We used datasets from the GEO database to identify important pathways in PE. We performed microarray profiling and functional analysis to identify differentially expressed long non-coding RNAs (lncRNAs), differentially expressed profiles of microRNA (miRNAs), and differentially expressed profiles of messenger RNA (mRNAs) in hypoxia-induced HTR8/SVneo cells. The candidates were validated using quantitative reverse transcription polymerase chain reaction. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses were performed to understand the functional significance of differentially expressed genes. Finally, we constructed an lncRNA-centered ceRNA network. Several hub genes were validated both in placentas from PE and normal pregnancy, and in hypoxia-induced HTR8/SVneo cells. The hypoxic response pathway was involved in the pathophysiology of PE. Subsequently, we identified 536 differentially expressed profiles of lncRNAs (183 upregulated and 353 downregulated), 46 differentially expressed profiles of miRNAs (35 upregulated and 11 downregulated), and 2782 differentially expressed profiles of mRNAs (DEmRNAs) (1031 upregulated and 1751 downregulated) in hypoxia-induced HTR8/SVneo cells. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed potential pathways affected by these genes, such as angiogenesis, the HIF-1 signaling pathway, and the PI3K-Akt signaling pathway. The ceRNA network comprised 35 lncRNAs, 11 miRNAs, 27 mRNAs, and 2 hub lncRNAs, which might play a vital role in placental functions and PE. Our results revealed the transcriptome profile and constructed an lncRNA-centered ceRNA network in hypoxia-induced HTR8/SVneo cells, thereby providing potential therapeutic targets for PE.