Intracerebral hemorrhage (ICH) refers to predominant, sporadic, and non-traumatic bleeding in the brain parenchyma. The PI3K/AKT/mTOR signaling pathway is an important signal transduction pathway regulated by enzyme-linked receptors and has many biological functions in mammals. It plays a key role in neuronal metabolism, gene expression regulation, and tissue homeostasis in the healthy and diseased brain.

In the present study, the role of the PI3K/AKT/mTOR pathway inhibitor chrysophanol (CPH) (10 mg/kg and 20 mg/kg, orally) in the improvement of ICH-associated neurological defects in rats was investigated. Autologous blood (20 µL/5 min/unilateral/intracerebroventricular) mimics ICH-like defects involving cellular and molecular dysfunction and neurotransmitter imbalance. The current study also included various behavioral assessments to examine cognition, memory, and motor and neuromuscular coordination. The protein expression levels of PI3K, AKT, and mTOR as well as myelin basic protein and apoptotic markers, such as Bax, Bcl-2, and caspase-3, were examined using ELISA kits. Furthermore, the levels of various neuroinflammatory cytokines and oxidative stress markers were assessed. Additionally, the neurological severity score, brain water content, gross brain pathology, and hematoma size were used to indicate neurological function and brain edema.

CPH was found to be neuroprotective by restoring neurobehavioral alterations and significantly reducing the elevated PI3K, AKT, and mTOR protein levels, and modulating the apoptotic markers such as Bax, Bcl-2, and caspase-3 in rat brain homogenate. CPH substantially reduced the inflammatory cytokines like interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. CPH administration restored the neurotransmitters GABA, glutamate, acetylcholine, dopamine, and various oxidative stress markers.

Our results show that CPH may be a promising therapeutic approach for overcoming neuronal damage caused by the overexpression of the PI3K/AKT/mTOR signaling pathway in ICH-induced neurological dysfunctions in rats.

The neuroprotective function of heat shock protein A5 (HSPA5) in ischemic stroke has been confirmed. This study aimed to investigate the effects of early aerobic exercise on neurological function recovery from cerebral ischemia/reperfusion and to determine whether these effects are associated with the expression level of HSPA5 in the ischemic penumbra.

A total of 72 male Sprague-Dawley rats were randomly assigned to the ischemia and exercise group [middle cerebral artery occlusion (MCAO)-Ex, n=18], ischemia and sedentary group (MCAO-St, n=18), sham-surgery and exercise group (Sham-Ex, n=18), or sham-surgery and sedentary group (Sham-St, n=18). The MCAO-Ex and MCAO-St groups were subjected to MCAO for 60 min, whereas the Sham-Ex and Sham-St groups were subjected to an identical operation without MCAO. Rats in the MCAO-Ex and Sham-Ex groups then ran on a treadmill for 30 min once a day for 5 consecutive days. After reperfusion, the motor function of the rats was scored by the Bederson neurological function test, balance beam test, and screen test. Nissl staining was conducted to assess morphological and structural change of nerve cells in the ischemic penumbra. The reverse transcription-quantitative polymerase chain reaction was applied to detect the mRNA expression of HSPA5. Western blot analysis was conducted to determine the protein expression of HSPA5. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining was carried out in the ischemic penumbra after MCAO.

Rats receiving early treadmill exercise had lower Bederson neurological function, balance beam, and screen test scores on the 3rd, 7th, and 14th days after MCAO; in addition, more neurons survived in the ischemic penumbra after MCAO, and higher mRNA and protein expression of HSPA5 and fewer TUNEL-positive stained cells were observed.

Our study demonstrated that early aerobic exercise can improve neurological function recovery after ischemia/reperfusion. Furthermore, the increased level of HSPA5 in the ischemic penumbra might be one of the mechanisms of enhanced neurological function recovery.

Fabry disease (FD) is an X-linked lysosomal storage disease caused by the mutation in the α-galactosidase A gene that leads to a consequently decreased α-galactosidase A enzyme activity and a series of clinical presentations. However, FD accompanied with aseptic meningitis can be relatively scarce and rarely reported, which leads to significant clinical misdiagnosis of this disease.

Sixteen patients diagnosed with FD based on a decreased activity of α-galactosidase A enzyme and/or genetic screening were identified through a 6-year retrospective chart review of a tertiary hospital. Clinical presentations, brain magnetic resonance imaging, cerebrospinal fluid analysis, treatment and outcome data were analyzed in cases of aseptic meningitis associated with FD.

Three out of 16 cases exhibited aseptic meningitis associated with FD. There was one female and two male patients with a mean age of 33.3 years. A family history of renal failure or hypertrophic cardiomyopathy was found in 3 cases. All cases presented with a persistent or intermittent headache and recurrent ischemic stroke. The cerebrospinal fluid analyses showed mild pleocytosis in 2 patients and an elevated level of protein in all patients. Cerebrospinal fluid cytology revealed activated lymphocytes, suggesting the existence of aseptic meningitis. In the literature review, up to 9 cases presenting with FD and aseptic meningitis were found, which bore a resemblance to our patients in demographic and clinical characteristics.

Our cases suggested that aseptic meningitis in FD might be under-detected and easily misdiagnosed, and should be more thoroughly examined in further cases.

Paroxysmal kinesigenic dyskinesia (PKD) is a rare movement disorder PRRT2 gene mutations have been reported to cause PKD. However, the pathophysiological mechanism of PKD remains unclear, and it is unknown whether an inflammatory response is involved in the occurrence of this disease. We aimed to investigate the symptomatology, genotype, and serum cytokines of patients with PKD.

We recruited 21 patients with PKD, including 7 with familial PKD and 14 with sporadic PKD. Their clinical features were investigated, and blood samples were collected, and PRRT2 mutations and cytokine levels were detected.

The mean age at PKD onset was 12.3±2.2 years old. Dystonia was the most common manifestation of dyskinesia, and the limbs were the most commonly affected parts. All attacks were induced by identifiable kinesigenic triggers, and the attack durations were brief (<1 min). Four different mutations from 9 probands were identified in 7 familial cases (71.4%) and 14 sporadic cases (28.6%). Two of these mutations (c.649dupC, c.620_621delAA) had already been reported, while other 2 (c.1018_1019delAA, c.1012+1G>A) were previously undocumented. The tumor necrosis factor (TNF)-α level in the PKD group was significantly higher than that in the age- and sex-matched control group (P=0.025). There were no significant differences in the interleukin (IL)-1β, IL-2R, IL-6, IL-8, or IL-10 levels between the two groups.

In this study, we summarized the clinical and genetic characteristics of PKD. We found that the serum TNF-α levels were elevated in patients clinically diagnosed with PKD, suggesting that an inflammatory response is involved in the pathogenesis of PKD.

To determine the impact of smoking on disease-specific health care utilization and medical costs in patients with chronic non-communicable diseases (NCDs).

Participants were middle-aged and elderly adults with chronic NCDs from a prospective cohort in China. Logistic regressions and linear models were used to assess the relationship between tobacco smoking, health care utilization and medical costs.

Totally, 1020 patients with chronic obstructive pulmonary disease (COPD), 3144 patients with coronary heart disease (CHD), and 1405 patients with diabetes were included in the analysis. Among patients with COPD, current smokers (β: 0.030, 95% CI: −0.032–0.092) and former smokers (β: 0.072, 95% CI: 0.014–0.131) had 3.0% and 7.2% higher total medical costs than never smokers. Medical costs of patients who had smoked for 21–40 years (β: 0.028, 95% CI:−0.038–0.094) and ≥41 years (β: 0.053, 95% CI: −0.004β0.110) were higher than those of never smokers. Patients who smoked ≥21 cigarettes (β: 0.145, 95% CI: 0.051–0.239) per day had more inpatient visits than never smokers. The association between smoking and health care utilization and medical costs in people with CHD group was similar to that in people with COPD; however, there were no significant associations in people with diabetes.

This study reveals that the impact of smoking on health care utilization and medical costs varies among patients with COPD, CHD, and diabetes. Tobacco control might be more effective at reducing the burden of disease for patients with COPD and CHD than for patients with diabetes.

To examine the independent risk factors of type-2 myocardial infarction (T2MI) elicited by acute upper gastrointestinal bleeding (AUGIB), and to establish a nomogram model for the prediction of AUGIB-induced T2MI.

A nomogram model was established on the basis of a retrospective study that involved 533 patients who suffered from AUGIB in the Department of Critical Care Medicine (CCM) or Emergency Intensive Care Unit (EICU) of Renmin Hospital of Wuhan University, Wuhan, China, from January 2017 to December 2020. The predictive accuracy and discriminative power of the nomogram were initially evaluated by internal validation, which involved drawing the receiver operating characteristic (ROC) curve, calculating the area under the curve (AUC), plotting the calibration curve derived from 1000 resampled bootstrap data sets, and computing the root mean square error (RMSE). The predictive ability of the nomogram was further validated through the prospective and multicenter study conducted by the investigators, which enrolled 240 AUGIB patients [including 88 cases from Renmin Hospital of Wuhan University, 73 cases from Qilu Hospital of Shandong University (Qingdao), and 79 cases from Northern Jiangsu People’s Hospital)], who were admitted to the Department of CCM or EICU, from February 2021 to July 2021.

Among the 533 patients in the training cohort, 78 (14.6%) patients were assigned to the T2MI group and 455 (85.4%) patients were assigned to the non-T2MI group. The multivariate analysis revealed that age >65, hemorrhagic shock, cerebral stroke, heart failure, chronic kidney disease, increased blood urea nitrogen, decreased hematocrit, and elevated D-Dimer were independent risk factors for AUGIB-induced T2MI. All these factors were incorporated into the nomogram model. The AUC for the nomogram for predicting T2MI was 0.829 (95% CI, 0.783–0.875) in the internal validation cohort and 0.848 (95% CI, 0.794–0.902) in the external validation cohort. The calibration curve for the risk of T2MI exhibited good consistency between the prediction by the nomogram and the actual clinical observation in both the internal validation (RMSE=0.016) and external validation (RMSE=0.020).

The nomogram was proven to be a useful tool for the risk stratification of T2MI in AUGIB patients, and is helpful for the early identification of AUGIB patients who are prone to T2MI for early intervention, especially in emergency departments and intensive care units.

Atherosclerosis is considered a chronic inflammatory condition. The immune system is a key mediator in the initiation and progression of atherosclerosis. In a previous study, we found that the immune system was activated in diabetes and that total white blood cell (WBC) counts were elevated significantly in diabetic patients. To investigate whether WBC subtype counts in newly diagnosed diabetes are risk factors for future cardiovascular disease (CVD) events, we conducted a prospective population-based cohort study.

A total of 1498 newly diagnosed diabetic patients aged 40 to 70 years old were followed up for three years. Participants with previous CVD history and abnormal WBC counts were excluded. CVD events were recorded during follow-up.

We found that the baseline lymphocyte counts were independently associated with cardiovascular events during follow-up, with the Exp (β) (95% CI) at 1.749 (1.084–2.821). Lymphocyte count ≥2.9 (10⁹/L) was significantly associated with the development of CVD (HR, 2.29; 95% CI, 1.12–4.67). The corresponding incidence of CVD per 1000 person-year for the lymphocyte count ≤2.8 (10⁹/L) and lymphocyte count ≥2.9 (10⁹/L) groups were 11.26 and 26.38, respectively.

We concluded that even in a normal range, higher lymphocyte levels may result in a significantly higher CVD risk among diabetic patients. Lymphocyte count ≥2.9 (10⁹/L) is an independent predictor of developing future CVD events.

S100A11 is a member of the S100 calcium-binding protein family and has intracellular and extracellular regulatory activities. We previously reported that S100A11 was differentially expressed in the respiratory tracts of asthmatic rats as compared with normal controls. Here, we aimed to analyze the potential of S100A11 to regulate both allergen-induced airway hyperresponsiveness (AHR) as well as acetylcholine (ACh)-induced hypercontractility of airway smooth muscle (ASM) and contraction of ASM cells (ASMCs).

Purified recombinant rat S100A11 protein (rS100A11) was administered to OVA-sensitized and challenged rats and then the AHR of animals was measured. The relaxation effects of rS100A11 on ASM were detected using isolated tracheal rings and primary ASMCs. The expression levels of un-phosphorylated myosin light chain (MLC) and phosphorylated MLC in ASMCs were analyzed using Western blotting.

Treatment with rS100A11 attenuated AHR in the rats. ASM contraction assays showed that rS100A11 reduced the contractile responses of isolated tracheal rings and primary ASMCs treated with ACh. In addition, rS100A11 markedly decreased the ACh-induced phosphorylation of the myosin light chain in ASMCs. Moreover, rS100A11 also suppressed the contractile response of tracheal rings in calcium-free buffer medium.

These results indicate that S100A11 protein can relieve AHR by relaxing ASM independently of extracellular calcium. Our data support the idea that S100A11 is a potential therapeutic target for reducing airway resistance in asthma patients.

The goal of this study is to investigate the role and mechanism of endoplasmic reticulum stress and apoptosis regulated by thrombospondin 1 (TSP1) in human renal tubular epithelial cells (HK-2 cells).

HK-2 cells were exposed to high concentrations of glucose (HG). The endoplasmic reticulum stress inhibitor 4-phenylbutyric acid (4-PBA) was administered by transfecting TSP1 or an empty vector to explore the mechanism of the endoplasmic reticulum response regulated by TSP1 and stress in renal cell apoptosis. The effects of TSP1 and 4-PBA on the proliferation and apoptosis of HK-2 cells under HG conditions were assessed using Cell counting kit-8 and flow cytometry. Western blotting was used to detect the apoptosis- and endoplasmic reticulum stress-related protein expression regulated by TSP1 and 4-PBA.

HG treatment induced high cell apoptosis, abundantly expressed TSP1 level and restrained viability in HK-2 cells. Overexpression of TSP1 significantly inhibited the proliferation of and facilitated apoptosis of HK-2 cells under HG conditions. Administration of endoplasmic reticulum stress inhibitor 4-PBA after overexpression of TSP1 antagonized the inhibitory proliferation and promoted apoptosis rate in HG-triggered HK-2 cells induced by TSP1 overexpression. 4-PBA treatment significantly hindered the expression of endoplasmic reticulum stress markers, such as PERK, ATF4, ATF6, p-eIF2α, IRE1, CHOP and XBP1, suggesting that the administration of 4-PBA was successful.

Overexpression of TSP1 activated endoplasmic reticulum stress by regulating the ATF6-CHOP axis. TSP1 restrained cell proliferation, and promoted apoptosis and endoplasmic reticulum stress by activating the ATF6-CHOP axis.

This study aimed to evaluate the relationships between the albumin/globulin ratio (AGR), neutrophil/lymphocyte ratio (NLR), and platelet/lymphocyte ratio (PLR) and clinicopathological information for gastric cancer patients. In addition, the prognostic values of these hematological parameters for resectable gastric cancer patients undergoing a total gastrectomy were determined.

A total of 245 patients with gastric cancer who underwent a total gastrectomy at our hospital between January 1, 2005, and December 30, 2015, were enrolled into this study. The preoperative AGR, NLR, and PLR in the serum samples of the patients were measured. The relationships between the hematological parameters and the disease-free survival (DFS) as well as overall survival (OS) were analyzed by statistical analysis.

The cutoff values of AGR, NLR, and PLR were 1.57, 3.5, and 193, respectively. Univariate analyses demonstrated that a low AGR, a high NLR, and a high PLR were significant risk factors for a poor prognosis. According to multivariate analysis, a high PLR was found to be independently associated with a poor survival. Additionally, when age was considered as a stratified factor, univariate analyses demonstrated that a low AGR had the tendency to be correlated with a shorter DFS in nonelderly patients (<65 years old). A low AGR was significantly correlated with a shorter DFS and OS in elderly patients (≥65 years old).

AGR, NLR, and PLR are independent risk factors associated with a poor gastric cancer survival by univariate analysis, and AGR is an independent risk factor for predicting DFS and OS in elderly patients (≥65 years old) with gastric cancer after total gastrectomy.

Gastric cancer (GC) is a deadly cancer and a challenging public health problem globally. This study aimed to analyze potential genes associated with pathogenesis and prognosis of gastric cancer.

This work selected the overlapping differentially expressed genes (DEGs) in GC from four datasets, the GSE29272, GSE29998, GSE54129 and GSE118916 Gene Expression Omnibus databases. These DEGs were used to carry out comprehensive bioinformatic analysis to analyze the related functions and pathways enriched, the relative expression levels and immune infiltrates, the prognostic characteristics and the interaction network.

In total, 55 DEGs increased while 98 decreased in their expression levels. For those DEGs with increased expression, they were mostly concentrated on “focal adhesion” and “ECM-receptor interaction”, whereas DEGs with decreased expression were mostly associated with “gastric acid secretion” and “drug metabolism cytochrome P450”. MCODE and ClueGO results were then integrated to screen 10 hub genes, which were FN1, COL1A1, COL3A1, BGN, TIMP1, COL1A2, LUM, VCAN, COL5A2 and SPP1. Survival analysis revealed that higher expression of the ten hub genes significantly predicted lower overall survival of GC patients. TIMP1 was most significantly related to neutrophils, CD8⁺ T cells, as well as dendritic cells, while LUM was most significantly related to macrophages.

Immunohistochemistry results and functional testing showed that the expression of COL5A2 was elevated in GC and that it might be a key gene in GC tumorigenesis.

This study aims to investigate the effect of ω-3 fatty acid immunonutritional therapy on natural killer (NK) cell gene methylation and function in elderly patients with gastric cancer.

A total of 70 cases of elderly patients with gastric cancer were randomized into the ω-3 fatty acid group and placebo group, according to the type of nutritional support administered. The methylation status of the tumor necrosis factor (TNF)-α gene promoter in peripheral NK cells was detected by methylation specific polymerase chain reaction, and the TNF-α level in peripheral NK cells was detected by enzyme-linked immunosorbent assay.

After 14 days of immunonutritional therapy with ω-3 fatty acid or placebo, patients in the ω-3 group had significantly higher average NK cell activity (0.27 vs. 0.24, P=0.013) and lower percentages of TNF-α gene promoter methylation (25.7% vs. 60%, P<0.05) than the placebo group. However, there were no significant differences in the concentration of albumin, prealbumin and TNF-α in serum, and the NK cell count between the ω-3 group and placebo group.

The postoperative application of ω-3 fatty acid may improve the activity of NK cells, which is correlated to the methylation status of the TNF-α gene promoter.

At present, a number of very severe aplastic anemia (VSAA) patients cannot receive hematopoietic stem cell transplantation (HSCT) or standard immunosuppressive therapy (IST) due to the high cost of therapy, shortage of sibling donors, and lack of resources to support the HSCT. In addition, some VSAA patients with autoantibodies have no life-threatening infections or bleeding at the time of initial diagnosis. Considering the disease condition, economics and other factors, the present study designed a new and relatively mild treatment strategy: cyclosporine A plus pulsed high-dose prednisone (CsA+HDP).

The present study retrospectively analyzed 11 VSAA patients, who were treated with CsA+HDP in our hospital from August 2017 to August 2019.

The median follow-up time for these patients was 24.9 months. The overall response rate was 54.5% (6/11) at six months after the initiation of IST and 81.8% (9/11) at deadline. Five patients achieved complete remission and four patients met the criteria for partial response at the last follow-up. The median time to response for responders was 110 days. Three patients underwent HSCT due to the poor effect of CsA+HDP or to find a suitable transplant donor. Recurrence and clonal evolution were not found in any of these patients. The estimated 3-year overall survival rate and 3-year failure-free survival rate were 100.0% and 72.7%, respectively. In addition, the results revealed that the cyclosporine-prednisone-associated toxicity was mild and well-tolerated by most patients.

The novel CsA+HDP regimen has good therapeutic effect and safety for VSAA patients with autoantibodies, who have no serious life-threatening infections or bleeding at the time of initial diagnosis.

Pituitary adrenocorticotropic hormone (ACTH)-secreting adenoma is a relatively intractable endocrine adenoma that can cause a range of severe metabolic disorders and pathological changes involving multiple systems. Previous studies have shown that celastrol has antitumor effects on a variety of tumor cells via the AKT/mTOR signaling. However, whether celastrol has pronounced antitumor effects on pituitary ACTH-secreting adenoma is unclear. This study aimed to identify a new effective therapeutic drug for pituitary ACTH-secreting adenoma.

Mouse pituitary ACTH-secreting adenoma cells (AtT20 cells) were used as an experimental model in vitro and to establish a xenograft tumor model in mice. Cells and animals were administered doses of celastrol at various levels. The effects of celastrol on cell viability, migration, apoptosis and autophagy were then examined. Finally, the potential involvement of AKT/mTOR signaling in celastrol’s mechanism was assessed.

Celastrol inhibited the proliferation and migration of pituitary adenoma cells in a time- and concentration-dependent manner. It blocked AtT20 cells in the G0/G1 phase, and induced apoptosis and autophagy by downregulating the AKT/mTOR signaling pathway. Similar results were obtained in mice.

Celastrol exerts potent antitumor effects on ACTH-secreting adenoma by downregulating the AKT/mTOR signaling in vitro and in vivo.

This study aimed to investigate the effects of downregulating astrocyte elevated gene-1 (AEG-1) expression combined with all-trans retinoic acid (ATRA) on vasculogenic mimicry (VM) formation and angiogenesis in glioma.

U87 glioma cells were transfected with AEG-1 shRNA lentiviral vectors (U87-siAEG-1) and incubated in a medium containing 20 µmol/L ATRA. Matrigel-based tube formation assay was performed to evaluate VM formation, and the cell counting kit-8 (CCK-8) assay was used to analyze the proliferation of glioma cells in vitro. Reverse transcription-quantitative polymerase chain reaction and Western blot analysis were used to investigate the mRNA and protein expression of related genes, respectively. Glioma xenograft models were generated via subcutaneous implantation of glioma cells in nude mice. Tumor-bearing mice received an intraperitoneal injection of ATRA (10 mg/kg per day). Immunohistochemistry was used to evaluate the expression of related genes and the microvessel density (MVD) in glioma xenograft models. CD34/periodic acid-Schiff double staining was performed to detect VM channels in vivo. The volume and weight of tumors were measured, and a tumor growth curve was drawn to evaluate tumor growth.

A combination of ATRA intervention and downregulation of AEG-1 expression significantly inhibited the proliferation of glioma cells in vitro and glioma VM formation in vitro and in vivo. It also significantly decreased MVD and inhibited tumor growth. Further, the expression levels of matrix metalloproteinase (MMP)-2, MMP-9, vascular endothelial-cadherin (VE-cadherin), and vascular endothelial growth factor (VEGF) in glioma significantly decreased in vivo and in vivo.

Hence, a combinatorial approach might be effective in treating glioma through regulating MMP-2, MMP-9, VEGF, and VE-cadherin expression.

Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), causes an estimated 1.6 million human deaths annually, but the pathogenesis of TB remains unclear. Immunity plays a critical role in the onset and outcome of TB. This study aimed to uncover the roles of innate and adaptive immunity in TB.

The gene expression profiles generated by RNA sequencing from human peripheral blood mononuclear cells (PBMCs) stimulated with or without Mtb strain H37Rv antigens were analyzed. A total of 973 differentially expressed mRNAs were identified.

The differentially expressed genes were enriched in innate immunity signaling functions. The mesenchymal-epithelial transition factor (MET) gene was significantly upregulated in CD14⁺ monocytes. A MET inhibitor improved the uptake of the BCG strain by monocytes and macrophages as well as inhibited the expression of indoleamine 2,3-dioxygenase (IDO). The expression of IDO was increased in PBMCs stimulated with Mtb antigens, and the IDO inhibitor promoted the expression of CD40, CD83, and CD86.

Our results might provide clues regarding the immunomodulatory mechanisms used by Mtb to evade the host defense system.

Previous studies have shown that the autonomic nervous system (ANS), which can be affected by emotions, is important in the occurrence or progression of glaucoma. The autonomic innervation distributed in the anterior chamber (AC) structures might play an efferent role in the neural regulation of intraocular pressure (IOP). This study aimed to investigate the anatomic neural connection from the emotional brain to autonomic innervation in the AC.

A retrograde trans-multisynaptic pseudorabies virus encoded with an enhanced green fluorescent protein (PRV531) and non-trans-synaptic tracer FAST Dil were injected into the right eye of mice, respectively. Fluorescent localization in the emotional brain and preganglionic nuclei was studied. Five and a half days after PRV531 injection into the right AC, fluorescent signals were observed in several emotional brain regions, including the amygdala, agranular insular cortex, lateral septal nuclei, periaqueductal gray, and hypothalamus. Autonomic preganglionic nuclei, including Edinger-Westphal nucleus, superior salivatory nucleus, and intermediolateral nucleus, were labeled using PRV531.

The sensory trigeminal nuclei were not labeled using PRV531. The fluorescence signals in the nuclei mentioned above showed bilateral distribution, primarily on the ipsilateral side. Seven days after injecting FAST Dil into the AC, we observed no FAST Dil-labeled neurons in the central nervous system.

Our results indicate a neural connection from the emotional brain to autonomic innervation in the AC, which provides anatomical support for the emotional influence of IOP via the ANS.

To validate and use the Chinese Version of the M. D. Anderson Symptom Inventory (MDASI-C) to assess the symptom burden of breast cancer patients in China.

A total of 342 breast cancer patients in China participated in this study. Their symptoms were investigated with the MDASI-C from November 2020 to February 2021, and the reliability and validity of this tool were evaluated, respectively. Cluster analysis and correlation analysis were also performed.

The Cronbach’s alpha coefficient values of the symptom and interference items were 0.827 and 0.880, respectively. Construct validity revealed a four-factor structure. The Kaiser—Meyer—Olkin value was 0.760. The Karnofsky Performance Status, treatment phase, and cancer stage of the patients were grouped, and the differences of scores within the groups were significant. In addition, the employment status, education level, and age of the patients were significantly correlated with the symptoms. The correlation analysis of the education level of the patients showed that most of the symptoms and interference items were reduced as the education level was increased. The top three symptoms were disturbed sleep (3.10±2.52), difficulty remembering (2.54±2.30), and fatigue (2.24±2.13). The clinical and biochemical indicators such as body mass index and neutral granulocyte lymphocyte ratio had effects on many symptoms. As the patients’ BMI increased, the patients’ pain, disturbed sleep, and difficulty remembering were aggravated, and numbness was alleviated.

The MDASI-C is a reliable and effective assessment tool to evaluate patients with breast cancer in China. The symptoms are related to many clinical and biochemical indicators.

This study aimed to analyze the fungal species of pathogens isolated from patients with superficial mucocutaneous mycosis from May 2007 to December 2018.

A retrospective analysis was carried out to determine the pathogenic fungi isolated from patients with superficial fungal infections in the Medical Mycology Clinical Laboratory, Department of Dermatology and Venereology, Union Hospital, from May 2007 to December 2018.

A total of 7639 strains were obtained, belonging to 21 genera and 36 species. They mainly consisted of Candida (3707/7639, 48.53%) and dermatophytes (3594/7639, 47.05%). The specimens were skin scales, nail shavings, secretions on the nail grooves, broken or diseased hair and dandruff, secretions or pseudomembrane of the external genitalia, and the oral mucosa. A total of 7300 patients were enrolled in this study, including 3301 males and 3999 females aged 2 months to 92 years old with a median age of 46.04 years old except for 633 patients whose ages were unknown. Two strains of different species were isolated from each of 339 patients at different body sites. The most frequent species were Trichophyton rubrum complex (2906/7639, 38.04%), Candida albicans (2619/7639, 34.28%), and unclassified Candida spp. Dermatophytes were mostly isolated from glabrous skin (2138/3594, 59.49%), with T. rubrum complex being the predominant species. Candida strains were most commonly isolated from mucosal sites (1979/3707, 53.39%), and C. albicans was the most prevalent causative agent.

The main distribution of pathogenic fungal species isolated from patients with superficial mycosis from 2007 to 2018 in Wuhan, Hubei province and the surrounding areas was that Candida slightly outnumbered dermatophytes. Among all of the isolated strains, T. rubrum complex was the most abundant.

Contrast-enhanced ultrasound (CEUS) is advantageous for evaluating microcirculation, and has been applied to assess arthritis in previous studies. However, CEUS examinations have not been studied for hemophilia arthritis. Hemophilia arthritis is different from other arthritis, because it is induced by spontaneous joint bleeding. Hence, CEUS may have special value in evaluating hemophilia arthritis. The present study assessed the value of CEUS in evaluating synovial hypertrophy and predicting recurrent joint bleeding in severe hemophilia A patients.

From August 2016 to January 2017, 81 severe hemophilia A patients, who were referred to our hospital for ultrasound joint assessment with conventional ultrasound, were enrolled. Among these 81 patients, 46 patients consented for CEUS examinations on the same day.

Compared to color Doppler flow imaging (CDFI), four more joints presented with a blood flow signal under CEUS mode. In addition, the synovial hypertrophy measured by CEUS was thicker than that measured by conventional ultrasound. The ultrasound scores (including the total grey-scale ultrasound score, joint effusion/hemarthrosis, synovial hypertrophy, CDFI semi-quantitative score, and CEUS semi-quantitative score) were significantly higher in the joint bleeding group than in the no joint bleeding group (P<0.05). Furthermore, these ultrasound scores were positively correlated with the joint bleeding frequency, and had the highest correlation with the CEUS score (r=0.620, P<0.05).

CEUS can more accurately assess the degree of synovial hypertrophy and vascularization, and diagnose synovitis, when compared to conventional ultrasound. In addition, CEUS appears to be essential for evaluating the possibility of recurrent joint bleeding, and providing more reliable evidence for individualized treatment.

To explore the clinical value of ultrasound shear wave elastography (SWE) and contrast-enhanced ultrasound (CEUS) in transrectal prostate biopsy.

A total of 54 patients (average age: 67.79±12.01 years) in the experimental group underwent transrectal prostate biopsy under the guidance of SWE, while 46 patients (average age: 69.22±11.54 years) in the control group underwent transrectal prostate biopsy guided by CEUS.

There were a total of 451 needles, with an average of 8.35±1.67 needles per patient in the experimental group, and a total of 462 needles, with an average of 10.04±1.33 needles per patient in the control group. The difference in puncture times between the two groups was statistically significant (P<0.05). There was no significant difference in the positive detection rate, sensitivity or specificity between the two groups (P>0.05), but there was a significant difference in the diagnostic accuracy between the two groups (P<0.05). The E_mean and E_max of prostate cancer were significantly higher in the experimental group than in benign prostatic hyperplasia (P<0.05). The receiver operating characteristic curve (ROC) analysis showed that the area under the ROC curve (AUC) of E_mean was 0.752 (S.E. =0.072, 95% CI=0.611–0.894, P=0.007), and the best cutoff value was 47.005 kPa.

In summary, both SWE- and CEUS-guided transrectal prostate biopsy can help find the focus and guide the puncture, and improve the positive detection rate.

This study explains the application number and funding rate of oncology projects undertaken by the National Natural Science Foundation of China (NSFC), with focus on tumor radiotherapy-related research over the past 11 years.

A stratified analysis was carried out on the application and funding status of tumor radiotherapy studies in different NSFC project categories, different research areas, and different tumor types. Research areas that required specific focus, such as immunology-related radiotherapy, multimodality imaging and radiomics, and post-radiotherapy organ injury, were separately analyzed.

The status and development trends of various related research fields were studied, and the research results were presented with the support of the NSFC, in order to provide reference for future applications and funding allocations.

The number of applications for funding increases every year. Although the total number of funded projects has also increased every year, the funding rate has decreased year by year. Projects on radiotherapy and immunization have been at the forefront in recent years, and the funding rate for these projects increases yearly.

Population genetic analysis based on genetic markers harbors valuable forensic applications. In this regard, it is informative and imperative to explore Han groups as they are the largest population of China. In particular, there is a largely underrepresented amount of information from recent decades regarding the southeast costal Han Chinese. Therefore, the aim of this study is to investigate the available genetic characteristics of the Han population living in the Jinjiang, Fujian Province, Southeastern China.

We sampled 858 saliva samples and used the commercially available Microreader™ Y Prime Plus ID System to identify population data of Y-short tandem repeat (STR) loci of this region.

A total of 822 different haplotypes were observed. The overall haplotype diversity, discriminatory power and haplotype match probability were 0.9999, 0.9999 and 0.0012, respectively.

Our results showed that the Jinjiang Han population was closely genetically related to Han groups of China. Overall, we identified a set of 37 Y-STRs that are highly polymorphic, and that can provide meaningful information in forensic practice and human genetic research.