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BACKGROUND: This study aimed to investigate the interactions among three core elements of respiratory infection-pathogen, lung microbiome, and host response-and their avocation with the severity and outcomes of Mycoplasma pneumoniae pneumonia (MPP) in children. METHODS: We prospectively collected bronchoalveolar lavage fluid from a cohort of 41 children with MPP, including general MPP (GMPP) and complicated MPP (CMPP), followed by microbiome and transcriptomic analyses to characterize the association among pathogen, lung microbiome, and host response and correlate it with the clinical features and outcomes. RESULTS: The lung microbiome of patients with CMPP had an increased relative abundance of Mycoplasma pneumoniae (MP) and reduced alpha diversity, with 76 differentially expressed species. Host gene analysis revealed a key module associated with neutrophil function and several inflammatory response pathways. Patients with a high relative abundance of MP, manifested by a specific lung microbiome and host response type, were more prone to CMPP and had a long imaging recovery time. CONCLUSION: Patients with CMPP have a more disrupted lung microbiome than those with GMPP. MP, lung microbiome, and host response interacts with each other and are closely related to disease severity and outcomes in children with MPP.
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Mycoplasma pneumoniae , Nitrobencenos , Compuestos Organofosforados , Neumonía por Mycoplasma , Niño , Humanos , Mycoplasma pneumoniae/genética , Transcriptoma , Neumonía por Mycoplasma/diagnóstico , Neumonía por Mycoplasma/genética , PulmónRESUMEN
INTRODUCTION: In patients with stroke, poststroke dysphagia (PSD) is a common complication that plays an important role in morbidity and mortality. The aim of this paper was to assess the prevalence and risk factors of PSD using a systemic review and meta-analysis. METHODS: PubMed, Embase, Cochrane Library, and Web of Science databases were systematically searched for potentially eligible studies published until September 2023. Further, the pooled incidence and risk factors for PSD were determined using a random-effects model. Overall, 58 studies involving 37,404 patients with acute stroke were selected for the meta-analysis. RESULTS: The pooled incidence of PSD in patients with acute stroke was 42% (95% confidence interval [CI]: 36-48%), which is the highest in South America (47%) and lowest in Asia (37%). Notably, older age (odds ratio [OR]: 2.13; 95% CI: 1.53-2.97; p < 0.001), hypertension (OR: 1.23; 95% CI: 1.06-1.44; p = 0.007), diabetes mellitus (OR: 1.22; 95% CI: 1.04-1.44; p = 0.014), stroke history (OR: 1.26; 95% CI: 1.04-1.53; p = 0.019), and atrial fibrillation (OR: 1.58; 95% CI: 1.02-2.44; p = 0.039) were found to be associated with an increased risk of PSD. Conversely, sex differences, smoking, alcoholism, obesity, hyperlipidemia, ischemic heart disease, stroke type, and the hemisphere affected were not associated with the risk of PSD. CONCLUSION: The abstract reports the prevalence of PSD in patients with acute stroke and identified potential risk factors for PSD, including older age, hypertension, diabetes mellitus, stroke history, and atrial fibrillation.
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Poststroke aphasia is an acquired language disorder and has been proven to have adverse effects on patients' social skills and quality of life. However, there are some inconsistencies in the neuroimaging studies investigating poststroke aphasia from the perspective of regional alterations. A meta-analysis has been employed to examine the common pattern of abnormal regional spontaneous brain activity in poststroke aphasia in the current study. Specifically, the Anisotropic effect-size version of seed-based d mapping was utilized, and 237 poststroke aphasia patients and 242 healthy controls (HCs) from 12 resting-state functional magnetic resonance imaging studies using amplitude of low-frequency fluctuations (ALFF), fractional ALFF, or regional homogeneity were included. The results showed that compared with HCs, patients with poststroke aphasia demonstrated increased regional spontaneous brain activity in the right insula, right postcentral gyrus, left cerebellar lobule IX, left angular gyrus, right caudate nucleus, left parahippocampal gyrus, and right supplementary motor area, and decreased regional spontaneous brain activity in the left cerebellar lobule VI, left median cingulate and paracingulate gyri, right cerebellar crus I, and left supplementary motor area. The study could provide further evidence for pathophysiological mechanism of poststroke aphasia and help find targets for treatment.
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Afasia , Calidad de Vida , Humanos , Imagen por Resonancia Magnética/métodos , Encéfalo/diagnóstico por imagen , Afasia/diagnóstico por imagen , Afasia/etiología , Mapeo Encefálico/métodosRESUMEN
OBJECTIVE: To investigate the relationship between the expression of PD-L1 in OSCC and the clinicopathological features and prognosis of patients. METHODS: We retrospectively analyzed the clinicopathological data and prognosis of 381 OSCC patients. Immunohistochemical staining was performed on OSCC tumor specimens, and the expression level of PD-L1 was evaluated according to the combined positive score (CPS). Kaplan-Meier analysis was used to identify the effect of PD-L1 expression and clinicopathological features on the prognosis of patients. Univariate and multivariate Cox regression analyses were conducted to determine the hazard factors affecting the prognosis of patients. RESULTS: PD-L1 overexpression was significantly associated with cervical lymph node metastasis (p = 0.018), worse clinical stage (p = 0.022), worse tumor differentiation (p = 0.046), and worse depth of invasion (DOI) (p = 0.003). Poorer clinical stage and degree of tumor differentiation were significantly associated with poorer OS and DSS in patients. PD-L1 expression was not associated with prognosis in patients with OSCC. CONCLUSIONS: High PD-L1 expression was significantly associated with higher tumor malignancy in OSCC patients. Poorer clinical stage and degree of tumor differentiation were associated with poor prognosis in OSCC patients. Our results may help clinicians develop more appropriate individualized treatment strategies for their patients, thus improving their outcomes.
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Objective: To assess the effectiveness of using mobile health platforms for continuous care in preventing and treating osteoporosis. Methods: 114 patients with osteoporosis admitted to Nantong First People's Hospital from March 2021 to June 2022 were recruited and assigned equally via random number table method to receive either routine care (namely education on osteoporosis disease, dietary guidance, exercise guidance, activity guidance, medication supervision, fall prevention, psychological care, and secondary health education at the time of discharge) (routine group) or mobile health platform-based continuity of care (continuity group), with 57 patients in each group. Outcome measures included treatment compliance, disease knowledge of osteoporosis (diet, exercise, risk factors), quality of life level, and care satisfaction. Results: All eligible patients were followed up for one year after discharge from the hospital. Patients with continuity of care showed higher treatment compliance and disease knowledge of diet, exercise, and risk factors than those with routine care (P = .004). Continuity of care was associated with significantly higher MOS 36-item short-form health survey (SF-36) scores (The SF-36 is a self-administered questionnaire containing 36 items that survey overall health status) and nursing satisfaction in patients versus routine care (P = .004). Conclusion: Mobile health platform-based continuity of care effectively enhances post-discharge compliance and knowledge of osteoporosis in patients with osteoporosis, thereby improving post-discharge quality of life and satisfaction with care. Multi-center studies involving diverse healthcare settings and patient populations would provide more robust evidence. Moreover, these findings highlight the potential benefits of incorporating mobile health platforms into the care continuum for osteoporosis patients. Also, by utilizing mobile health platforms, healthcare providers can extend their reach beyond hospital settings and provide continuous care and support to patients, potentially reducing the burden on healthcare systems and improving overall population health outcomes.
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Triple-negative breast cancer (TNBC) remains the most challenging breast cancer subtype due to its lack of targeted therapies and poor prognosis. In order to treat patients with these tumors, efforts have been made to explore feasible targets. Epidermal growth factor receptor (EGFR)-targeted therapy is currently in clinical trials and regarded to be a promising treatment strategy. In this study, an EGFR-targeting nanoliposome (LTL@Rh2@Lipo-GE11) using ginsenoside Rh2 as a wall material was developed, in which GE11 was used as the EGFR-binding peptide to deliver more ginsenoside Rh2 and luteolin into TNBC. In comparison to non-targeted liposomes (Rh2@Lipo and LTL@Rh2@Lipo), the nanoliposomes LTL@Rh2@Lipo-GE11 demonstrated a high specificity to MDA-MB-231 cells that expressed a high level of EGFR both in vitro and in vivo, contributing to the strong inhibitory effects on the growth and migration of TNBC. These results suggest that LTL@Rh2@Lipo-GE11 is a prospective candidate for targeted therapy of TNBC, with a remarkable capability to inhibit tumor development and metastasis.
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Ginsenósidos , Neoplasias de la Mama Triple Negativas , Humanos , Liposomas/uso terapéutico , Neoplasias de la Mama Triple Negativas/metabolismo , Receptores ErbB/metabolismo , Ginsenósidos/farmacología , Ginsenósidos/uso terapéutico , Línea Celular TumoralRESUMEN
Tumor necrosis factor-alpha (TNF-α) plays an important pathogenic role in cardiac hypertrophy and heart failure (HF); however, anti-TNF is paradoxically negative in clinical trials and even worsens HF, indicating a possible protective role of TNF-α in HF. TNF-α exists in transmembrane (tmTNF-α) and soluble (sTNF-α) forms. Herein, we found that TNF receptor 1 (TNFR1) knockout (KO) or knockdown (KD) by short hairpin RNA or small interfering RNA (siRNA) significantly alleviated cardiac hypertrophy, heart dysfunction, fibrosis, and inflammation with increased tmTNF-α expression, whereas TNFR2 KO or KD exacerbated the pathological phenomena with increased sTNF-α secretion in transverse aortic constriction (TAC)- and isoproterenol (ISO)-induced cardiac hypertrophy in vivo and in vitro, respectively, indicating the beneficial effects of TNFR2 associated with tmTNF-α. Suppressing TNF-α converting enzyme by TNF-α Protease Inhibitor-1 (TAPI-1) to increase endogenous tmTNF-α expression significantly alleviated TAC-induced cardiac hypertrophy. Importantly, direct addition of exogenous tmTNF-α into cardiomyocytes in vitro significantly reduced ISO-induced cardiac hypertrophy and transcription of the pro-inflammatory cytokines and induced proliferation. The beneficial effects of tmTNF-α were completely blocked by TNFR2 KD in H9C2 cells and TNFR2 KO in primary myocardial cells. Furthermore, we demonstrated that tmTNF-α displayed antihypertrophic and anti-inflammatory effects by activating the AKT pathway and inhibiting the nuclear factor (NF)-κB pathway via TNFR2. Our data suggest that tmTNF-α exerts cardioprotective effects via TNFR2. Specific targeting of tmTNF-α processing, rather than anti-TNF therapy, may be more useful for the treatment of hypertrophy and HF.
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Cardiomegalia/metabolismo , Receptores Tipo II del Factor de Necrosis Tumoral/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Animales , Apoptosis/efectos de los fármacos , Cardiomegalia/fisiopatología , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Noqueados , Miocitos Cardíacos/metabolismo , FN-kappa B/metabolismo , Receptores Tipo I de Factores de Necrosis Tumoral/genética , Receptores Tipo I de Factores de Necrosis Tumoral/metabolismo , Receptores Tipo II del Factor de Necrosis Tumoral/genética , Receptores Tipo II del Factor de Necrosis Tumoral/fisiología , Transducción de Señal/efectos de los fármacos , Factor de Necrosis Tumoral alfa/fisiologíaRESUMEN
Background: Chondroblastoma is a primary bone tumor typically arising from the intramedullary space of the epiphysis or epimetaphysis. A non-epiphyseal chondroblastoma is uncommon. Case report: An 11-year-old girl presented with an eccentric cortical osteolytic lesion in the distal femur metaphysis. The typical morphology, diffuse H3.3 K36M immunohistochemical expression and H3F3B point mutation (c. 110A > T) unequivocally supported the diagnosis of chondroblastoma. Discussion: We described a non-epiphyseal cortical-based chondroblastoma involving the distal femur harboring the typical H3F3B mutation. Non-epiphyseal chondroblastoma may harbor the H3F3B mutation.
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Neoplasias Óseas , Condroblastoma , Niño , Femenino , Humanos , Neoplasias Óseas/diagnóstico , Condroblastoma/diagnóstico , Condroblastoma/genética , Condroblastoma/patología , Epífisis/metabolismo , Epífisis/patología , Fémur , MutaciónRESUMEN
To describe the clinical features and risk factors of device-related pressure injuries (DRPIs) in the operating room. The clinical features of the DRPIs in patients undergoing elective surgery in a tertiary hospital in 2020 were investigated through prospective data collection. A DRPI-related questionnaire was designed for the patients, and those who did not experience any DRPI were selected according to a ratio of 1:2. Logistic regression analysis was performed in terms of the independent risk factors of operating-room DRPIs. A P-value of <.05 indicated a statistically significant difference. The incidence of operating-room DRPIs was 0.56%, and the proportion of stage I injuries was 73.53%. The injury-related devices included vital monitoring devices (31.62%), auxiliary therapy devices (27.94%), therapy devices (19.12%), and dressings (3.67%). Non-bone protuberances, such as the upper arms and thighs, were common injury sites. The patients' body mass index, mean arterial pressure, and instrument action time were independent risk factors for the operating-room DRPIs. To reduce the incidence of operating-room DRPIs, it is of great clinical significance to focus on the characteristics of the surgical patients and the types of surgery-related devices used and to take personalised preventive measures based on the relevant risk factors.
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Úlcera por Presión , Humanos , Úlcera por Presión/epidemiología , Úlcera por Presión/etiología , Úlcera por Presión/prevención & control , Quirófanos , Factores de Riesgo , Vendajes/efectos adversos , IncidenciaRESUMEN
This survey aimed to describe the health-related quality of life (HRQoL) and to explore the relationship between chronic diseases and HRQoL among urban residents in Shanghai, China. A cross-sectional study of 9 426 adults was conducted in Xuhui District of Shanghai, China in 2015. The EuroQol five-dimension three-level (EQ-5D-3 L) was used to measure HRQoL. The average age of subjects was 55.6 ± 17.4 years and 53% were female. Their mean values of utility and visual analogue scale (VAS) were 0.974 ± 0.099 and 80.00 ± 12.36, respectively, which were above the Chinese norm values. Women had lower scores compared with men. The utility value decreased with age, which accelerated after the age of 55 years. Chronic conditions including diabetes, tumor, cardiovascular disease, and respiratory disease, were significantly related to HRQoL, and the reported proportions of problems in the five dimensions increased with the number of chronic diseases (p < 0.05). Chronic diseases except for respiratory disease had a negative effect on HRQoL utility value and VAS score after the adjustment for covariates (p < 0.05). Chronic diseases had a negative impact on both EQ-5D-3 L utility and VAS scores, although the health-related quality of life for the study was above the national average.
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Enfermedad Crónica , Calidad de Vida , Salud Urbana , Población Urbana , Adulto , Anciano , China/epidemiología , Enfermedad Crónica/epidemiología , Estudios Transversales , Femenino , Humanos , Masculino , Persona de Mediana Edad , Encuestas y Cuestionarios , Salud Urbana/estadística & datos numéricosRESUMEN
Asthma is defined as a heterogeneous disease, usually characterized by chronic airway inflammation. Long noncoding RNAs (lncRNAs) play important roles in various biological processes. To know more about the relationships between lncRNAs and asthma, gene microarray analysis was performed to screen differentially expressed lncRNAs between the lung tissue of ovalbumin (OVA) mice and control mice. Further studies showed that downregulating differentially expressed lncRNA-AK149641 by adeno-associated virus 6 (AAV6) in OVA mice inhibited airway inflammation, with improved airway compliance and resistance, diminished infiltration of inflammatory cells, as well as less secretions of mucus, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). Moreover, the activity of nuclear factor-kappa B (NF-κB) in the lung tissue was reduced after downregulating lncRNA-AK149641. In conclusion, we proposed that downregulation of lncRNA-AK149641 attenuated the airway inflammatory response in an OVA-induced asthma mouse model, probably in association with modulation of the NF-κB signaling pathway.
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Asma/genética , ARN Largo no Codificante/metabolismo , Animales , Asma/patología , Modelos Animales de Enfermedad , Femenino , Ratones , Ratones Endogámicos BALB C , OvalbúminaRESUMEN
Chronic neuroinflammation is a characteristic of Parkinson's disease (PD). Previous investigations have shown that Parkin gene mutations are related to the early-onset recessive form of PD and isolated juvenile-onset PD. Further, Parkin plays important roles in mitochondrial quality control and cytokine-induced cell death. However, whether Parkin regulates other cellular events is still largely unknown. In this study, we performed overexpression and knockout experiments and found that Parkin negatively regulates antiviral immune responses against RNA and DNA viruses. Mechanistically, we show that Parkin interacts with tumor necrosis factor receptor-associated factor 3 (TRAF3) to regulate stability of TRAF3 protein by promoting Lys48-linked ubiquitination. Our findings suggest that Parkin plays a novel role in innate immune signaling by targeting TRAF3 for degradation and maintaining the balance of innate antiviral immunity.
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Fibroblastos/inmunología , Inmunidad Innata , Transducción de Señal/inmunología , Factor 3 Asociado a Receptor de TNF/genética , Ubiquitina-Proteína Ligasas/genética , Animales , Células de la Médula Ósea/citología , Células de la Médula Ósea/inmunología , Células de la Médula Ósea/virología , Chlorocebus aethiops , Fibroblastos/citología , Fibroblastos/virología , Regulación de la Expresión Génica , Células HEK293 , Células HeLa , Herpesvirus Humano 1/inmunología , Humanos , Ratones , Mitocondrias/inmunología , Mitocondrias/metabolismo , Plásmidos/química , Plásmidos/metabolismo , Cultivo Primario de Células , Proteolisis , Virus Sendai/inmunología , Factor 3 Asociado a Receptor de TNF/inmunología , Transducción Genética , Ubiquitina-Proteína Ligasas/inmunología , Ubiquitinación , Células Vero , Vesiculovirus/inmunologíaRESUMEN
E3 ubiquitin ligase c-Caritas B cell lymphoma (c-cbl) is associated with negative regulation of receptor tyrosine kinases, signal transduction of antigens and cytokine receptors, and immune response. However, the expression and function of c-cbl in the regulation of neuropathic pain after chronic constriction injury (CCI) are unknown. In rat CCI model, c-cbl inhibited the activation of spinal cord microglia and the release of pro-inflammatory factors including tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1ß) and interleukin 6 (IL-6), which alleviated mechanical and heat pain through down-regulating extracellular signal-regulated kinase (ERK) pathway. Additionally, exogenous TNF-α inhibited c-cbl protein level vice versa. In the primary microglia transfected with c-cbl siRNA, when treated with TNF-α or TNF-α inhibitor, the corresponding secretion of IL-1ß and IL-6 did not change. In summary, CCI down-regulated c-cbl expression and induced the activation of microglia, then activated microglia released inflammatory factors via ERK signaling to cause pain. Our data might supply a novel molecular target for the therapy of CCI-induced neuropathic pain.
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Microglía/efectos de los fármacos , Neuralgia/fisiopatología , Traumatismos de los Nervios Periféricos/fisiopatología , Proteínas Proto-Oncogénicas c-cbl/fisiología , Médula Espinal/fisiopatología , Animales , Secuencia de Bases , Constricción , Regulación hacia Abajo/efectos de los fármacos , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Sistema de Señalización de MAP Quinasas/fisiología , Masculino , Fosforilación/fisiología , Proteínas Proto-Oncogénicas c-cbl/genética , Ratas Sprague-Dawley , Nervio Ciático/lesiones , Factor de Necrosis Tumoral alfa/farmacologíaRESUMEN
Columnar cell variant of papillary thyroid carcinoma (CCV-PTC) is an unusual neoplasm, the clinical behavior of which mainly depends on the encapsulation or infiltration. Patients with extensive extrathyroidal extension usually have an aggressive biological behavior. This study confirmed that beta-human chorionic gonadotropin (ß-hCG) secreting invasive CCV-PTC has good prognosis comparing with a cohort of follicular cell differentiated thyroid carcinoma. On the contrary, positive immunoreaction with ß-hCG was proved in three anaplastic thyroid carcinoma patients showing aggressive clinical courses. The clinicopathologic characteristics of CCV-PTC and the paraneoplastic syndromes in follicular cell differentiated thyroid carcinoma were further summarized using literature review.
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Adenocarcinoma Folicular/patología , Carcinoma Papilar/patología , Gonadotropina Coriónica Humana de Subunidad beta/biosíntesis , Neoplasias de la Tiroides/patología , Adenocarcinoma Folicular/metabolismo , Adenocarcinoma Folicular/mortalidad , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores de Tumor/análisis , Carcinoma Papilar/metabolismo , Carcinoma Papilar/mortalidad , Femenino , Humanos , Estimación de Kaplan-Meier , Masculino , Persona de Mediana Edad , Pronóstico , Cáncer Papilar Tiroideo , Neoplasias de la Tiroides/metabolismo , Neoplasias de la Tiroides/mortalidad , Adulto JovenRESUMEN
Spinal cord injury (SCI) is one of the most common and severe complications in spine injury. It is difficult to prevent cell necroptosis and promote the survival of residual neurons after SCI. Proteasome beta-4 subunit (PSMB4) is the first proteasomal subunit with oncogenic properties promoting cancer cell survival and tumor growth in vivo, and our previous study showed that PSMB4 is significantly associated with neuronal apoptosis in neuroinflammation. However, PSMB4 function in the necroptosis after SCI is unkown. RIP3, a key regulatory factor of necroptosis, correlates with the induction of necroptosis in various types of cells and signaling pathway. Upregulation of the RIP3 expression may play a role as a novel molecular mechanism in secondary neural tissue damage following SCI. In this study, we established an acute spinal cord contusion injury model in adult rats to investigate the potential role of PSMB4 during the pathological process of SCI. We found PSMB4 expression was significantly up-regulated 3 days after injury by western blot and immunohistochemical staining. Double immunofluorescent staining indicated obvious changes of PSMB4 expression occurred in neurons. Significant up-regulation of PSMB4 expression was observed in Rip3 positive neurons at 3 days after SCI, which indicated that PSMB4 might play a vital role in the regulation of Rip3. Overexpress and knockdown PSMB4 could intervene the RIP3 and Mixed lineage kinase domain-like protein (MLKL) pathway in Tumor necrosis factor-α (TNF-α) induced necroptosis cell model. Based on our experimental data, we boldly conclude that PSMB4 is associated with RIP3 involved necroptosis after SCI.
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Apoptosis/fisiología , Neuronas/metabolismo , Complejo de la Endopetidasa Proteasomal/metabolismo , Proteína Serina-Treonina Quinasas de Interacción con Receptores/metabolismo , Traumatismos de la Médula Espinal/metabolismo , Animales , Modelos Animales de Enfermedad , Masculino , Necrosis , Ratas Sprague-Dawley , Transducción de Señal/fisiología , Traumatismos de la Médula Espinal/fisiopatología , Activación Transcripcional/fisiología , Regulación hacia ArribaRESUMEN
BACKGROUND: Breast cancer is the most common cancer in women worldwide. However, it remains a difficult diagnosis problem to differentiate between benign and malignant breast lesions, especially in small early breast lesions. PURPOSE: To assess the diagnostic value of diffusion-weighted imaging (DWI) combined with T2-weighted imaging (T2WI) for small breast cancer characterization. MATERIAL AND METHODS: Fifty-eight patients (65 lesions) with a lesion <2 cm in diameter underwent 3.0 Tesla breast magnetic resonance imaging (MRI) including DWI and histological analysis. Three observers with varying experience levels reviewed MRI. The probability of breast cancer in each lesion on MR images was recorded with a 5-point scale. Areas under the receiver-operating characteristic curve (AUCs) were compared by using the Z test; sensitivity and specificity were determined with the Z test after adjusting for data clustering. RESULTS: AUC of T2WI and DWI (Observer 1, 0.95; Observer 2, 0.91; Observer 3, 0.83) was greater than that of T2WI (Observer 1, 0.80; Observer 2, 0.74; Observer 3, 0.70) for all observers (P < 0.0001 in all comparisons). Sensitivity of T2WI and DWI (Observer 1, 90%; Observer 2, 93%; and Observer 3, 86%) was greater than that of T2WI alone (Observer 1, 76%; Observer 2, 83%; Observer 3, 79%) for all observers (P < 0.0001 in all comparisons). Specificity of T2WI and DWI was greater than that of T2WI alone for observer 1 (89% vs. 72%, P < 0.01) and observer 2 (94% vs. 78%, P < 0.001). CONCLUSION: DWI combined with T2WI can improve the diagnostic performance of MRI in small breast cancer characterization. It should be considered selectively in the preoperative evaluation of patients with small lesions of the breast.
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Neoplasias de la Mama/diagnóstico , Imagen por Resonancia Magnética/métodos , Adulto , Anciano , Neoplasias de la Mama/patología , Diagnóstico Diferencial , Imagen de Difusión por Resonancia Magnética , Femenino , Humanos , Mamografía , Persona de Mediana Edad , Ultrasonografía MamariaRESUMEN
Jinlida granule (JLD) is a Traditional Chinese Medicine (TCM) formula used for the treatment of type 2 diabetes mellitus (T2DM). However, the mechanism of JLD treatment for T2DM is not fully revealed. In this study, we explored the mechanism of JLD against T2DM by an integrative pharmacology strategy. Active components and corresponding targets were retrieved from Traditional Chinese Medicine System Pharmacology (TCMSP), SwissADME and Bioinformatics Analysis Tool for Molecular Mechanisms of Traditional Chinese Medicine Database (BATMAN-TCM) database. T2DM-related targets were obtained from Drugbank and Genecards databases. The protein-protein interaction (PPI) network was constructed and analyzed with STRING (Search Toll for the Retrieval of Interacting Genes/proteins) and Cytoscape to get the key targets. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) enrichment analyses were performed with the Database for Annotation, Visualization and Integrated Discovery (DAVID). Lastly, the binding capacities and reliability between potential active components and the targets were verified with molecular docking and molecular dynamics simulation. In total, 185 active components and 337 targets of JLD were obtained. 317 targets overlapped with T2DM-related targets. RAC-alpha serine/threonine-protein kinase (AKT1), tumor necrosis factor (TNF), interleukin-6 (IL-6), cellular tumor antigen p53 (TP53), prostaglandin G/H synthase 2 (PTGS2), Caspase-3 (CASP3) and signal transducer and activator of transcription 3 (STAT3) were identified as seven key targets by the topological analysis of the PPI network. GO and KEGG enrichment analyses showed that the effects were primarily associated with gene expression, signal transduction, apoptosis and inflammation. The pathways were mainly enriched in PI3K-AKT signaling pathway and AGE-RAGE signaling pathway in diabetic complications. Molecular docking and molecular dynamics simulation verified the good binding affinity between the key components and targets. The predicted results may provide a theoretical basis for drug screening of JLD and a new insight for the therapeutic effect of JLD on T2DM.
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Diabetes Mellitus Tipo 2 , Medicamentos Herbarios Chinos , Simulación del Acoplamiento Molecular , Mapas de Interacción de Proteínas , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Medicamentos Herbarios Chinos/farmacología , Medicamentos Herbarios Chinos/química , Humanos , Mapas de Interacción de Proteínas/efectos de los fármacos , Transducción de Señal/efectos de los fármacos , Medicina Tradicional China/métodos , Simulación de Dinámica Molecular , Biología Computacional/métodos , Ontología de Genes , Hipoglucemiantes/farmacología , Hipoglucemiantes/químicaRESUMEN
Anaplastic thyroid carcinoma (ATC) is the most advanced and aggressive thyroid cancer, and poorly differentiated thyroid carcinoma (PDTC) lacks anaplastic histology but has lost architectural and cytologic differentiation. Only a few studies have focused on the genetic relationship between the two advanced carcinomas and coexisting differentiated thyroid carcinomas (DTCs). In the present study, we investigated clinicopathologic features and genetic profiles in 57 ATC and PDTC samples, among which 33 cases had concomitant DTC components or DTC history. We performed immunohistochemistry for BRAF V600E, p53, and PD-L1 expression, Sanger sequencing for TERT promoter and RAS mutations, and fluorescence in situ hybridization for ALK and RET rearrangements. We found that ATCs and PDTCs shared similar gene alterations to their coexisting DTCs, and most DTCs were aggressive subtypes harboring frequent TERT promoter mutations. A significantly higher proportion of ATCs expressed p53 and PD-L1, and a lower proportion expressed PAX-8 and TTF-1, than the coexisting DTCs. Our findings provide more reliable evidence that ATCs and PDTCs are derived from DTCs.
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Adenocarcinoma , Síndrome de Ehlers-Danlos , Prolina/análogos & derivados , Tiocarbamatos , Neoplasias de la Tiroides , Humanos , Antígeno B7-H1 , Hibridación Fluorescente in Situ , Proteína p53 Supresora de Tumor/genética , Neoplasias de la Tiroides/genéticaRESUMEN
The purpose of this study is to systematically analyze the development trend, research hotspots, and future development direction on the treatment of neuropathic pain (NP) with spinal cord stimulation through bibliometric method. We extracted the literature related to the treatment of NP with spinal cord stimulation from January 2004 to December 2023 from the Web of Science database. As a result, a total of 264 articles were retrieved. By analyzing the annual published articles, authors, countries, institutions, journals, co-cited literature, and keywords, we found that the count of publication in this field has been experiencing an overall growth, and the publications within the past 5 years accounted for 42% of the total output. Experts from the United States and the UK have made significant contributions in this field and established a stable collaborative team, initially establishing an international cooperation network. Pain is the frequently cited journal in this field. The study on spinal cord stimulation therapy for NP especially the study on spinal cord stimulation therapy for back surgery failure syndrome (FBSS) and its potential mechanisms are the research hotspots in this field, while the study on novel paradigms such as high-frequency spinal cord stimulation and spinal cord burst stimulation represents the future development directions. In short, spinal cord stimulation has been an effective treatment method for NP. The novel paradigms of spinal cord stimulation are the key point of future research in this field.
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The aim of this study is to describe the general information, disease and treatment of venous thromboembolism (VTE) in critically ill patients, to explore the characteristics of severe patients with deep venous VTE and provide clinical reference data for the prevention and treatment of VTE in critically ill patients. This study carried out a retrospective study on the medical records of patients who were treated in the intensive care unit of Affiliated Hospital of Jining Medical College from 2020 to 2022. The general data, general conditions, drug use, past history, VTE prevention measures, post-VTE conditions, and Padua risk score of 297 patients with VTE during the period of hospitalization in intensive care unit (ICU) were classified and statistically analyzed. A total of 297 including 171 male and 126 male patient medical records were included in the analysis, we compared multiple clinical indicators between male and female patients. Compared to women, male patients have a higher acute physiology and chronic health evaluation II score(APACHE-II score) (Pâ =â .027), a higher state of consciousness (Pâ =â .003), a higher rate of smoking and drinking history (Pâ <â .001), a lower rate of heart failure (Pâ =â .003) and chronic depression (Pâ =â .013), and a higher rate of recommended operations for male patients after VTE (Pâ =â .031). The prothrombin time (PT) (Pâ =â .041) and activated partial thromboplastin time (APTT) (Pâ =â .040) of male patients were significantly higher than those of female patients, while triglyceride (Pâ =â .009) and total cholesterol (TC) (Pâ =â .001) were significantly lower than those of female patients. The difference in D-dimer (Pâ =â .739) was not significant. This study shows that male and female patients with VTE in the ICU have significant differences in general characteristics, general clinical conditions, history of past illness, thrombosis character, and examination items, this may be the reason for the different rates of VTE between male and female patients in the ICU.