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BACKGROUND: Whole-brain radiotherapy (WBRT) is a standard and effective approach for brain metastases, but it is linked to neurocognitive complications, specifically issues related to the hippocampus. Innovative strategies are being explored to enhance outcomes. However, a consensus is yet to be reached in this field. Our aim is to investigate the efficacy and safety of WBRT combined with simultaneous integrated boost (SIB), memantine, and hippocampal avoidance (HA) techniques in treatment of brain metastases. METHODS: In this systematic review and meta-analysis, we comprehensively searched PubMed, MEDLINE, Embase, and Cochrane for studies reporting the efficacy and toxicity of WBRT-based combination therapies from inception to September 19, 2023. Data were pooled using random-effects models. Results were reported as risk ratios (RRs) and risk differences (RDs) for dichotomous outcomes, along with their 95% confidence intervals (CIs). Heterogeneity was evaluated using the I2 statistic. RESULTS: Among 2175 articles, 29 studies involving 3460 patients were included. The meta-analysis revealed that compared to WBRT alone, combination therapies significantly mitigated neurocognitive function decline (RD = -0.09, 95% CI [-0.18-0.01]; P = 0.03) and intracranial control failure (RR = 0.86, 95% CI [0.52-1.44]; P = 0.02), without increasing the risk of hippocampal recurrence or high-grade toxicities. Notably, HA-WBRT + SIB/memantine demonstrated improved neurocognitive outcomes and survival benefits. CONCLUSION: WBRT-based combination therapies demonstrate improved efficacy and comparable safety to WBRT alone, with specific emphasis on the effectiveness of HA-WBRT + Memantine and HA-WBRT + SIB in optimizing therapeutic outcomes for brain metastases.

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INTRODUCTION AND OBJECTIVES: Breast and non-small cell lung cancers harbor an upregulated CSNK2A2 oncogene that encodes the protein kinase CK2 alpha', a catalytic subunit of the highly conserved serine/threonine kinase CK2. However, its role and biological significance in hepatocellular carcinoma (HCC) remains unclear. MATERIALS AND METHODS: Western-blotting and immunohistochemistry were used to measure the expression of CSNK2A2 in HCC tumor tissues and cell lines. CCK8, Hoechst staining, transwell, tube formation assay in vitro and nude mice experiments in vivo were used to measure the effects of CSNK2A2 on HCC proliferation, apoptosis, metastasis, angiogenesis and tumor formation. RESULTS: In the study, we showed that CSNK2A2 was highly expressed in HCC comparison with matched control tissues, and was linked with lower survival of patients. Additional experiments indicated that silencing of CSNK2A2 promoted HCC cell apoptosis, while inhibited HCC cells migrating, proliferating, angiogenesis both in vitro and in vivo. These effects were also accompanied by reduced expression of NF-κB target genes, including CCND1, MMP9 and VEGF. Moreover, treatment with PDTC counteracted the promotional effects of CSNK2A2 on HCC cells. CONCLUSIONS: Overall, our results suggested that CSNK2A2 could promote HCC progression by activating the NF-κB pathway, and this could serve as a biomarker for future prognostic and therapeutic applications.

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Pancreatic cancer (PAC) is one of the most lethal malignant neoplasms with poor prognosis and high mortality. Emerging evidence has revealed that abnormal tumor lipid metabolism and tumor-associated macrophages (TAMs) significantly contribute to PAC development and progression. Therefore, concurrently reprogramming tumor lipid metabolism and regulating TAMs function could be a promising strategy for effective PAC therapy. Herein, we identified an important enzyme catabolizing lipids (monoacylglycerol lipase, MGLL) and a key receptor regulating macrophage phenotype (endocannabinoid receptor-2, CB-2) that are over-expressed in PAC cells and on TAMs, respectively. Based on this finding, we developed a reduction-responsive poly (disulfide amide) (PDSA)-based nanoplatform for systemic co-delivery of MGLL siRNA (siMGLL) and CB-2 siRNA (siCB-2). This nanoplatform could utilize its reduction-responsive characteristic to rapidly release siRNA for efficient silencing of MGLL and CB-2, inducing concurrent suppression of free fatty acids (FFAs) generation in PAC cells and repolarization of TAMs into tumor-inhibiting M1-like phenotype. With this suppressed FFAs generation to inhibit nutrient supply for tumor cells and repolarized TAMs to secrete tumoricidal cytokines such as TNF-α and IL-12, a combinational anticancer effect could be achieved in both xenograft and orthotopic PAC tumor models.

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GM2 gangliosidosis, Tay-Sachs and Sandhoff diseases, are lysosomal storage disorders characterized by the lysosomal accumulation of GM2 gangliosides. This accumulation is due to deficiency in the activity of the ß-hexosaminidases Hex-A or Hex-B, which are dimeric hydrolases formed by αß or ßß subunits, respectively. These disorders show similar clinical manifestations that range from mild systemic symptoms to neurological damage and premature death. There is still no effective therapy for GM2 gangliosidoses, but some therapeutic alternatives, as enzyme replacement therapy, have being evaluated. Previously, we reported the production of active human recombinant ß-hexosaminidases (rhHex-A and rhHex-B) in the methylotrophic yeast Pichia pastoris. In this study, we evaluated in vitro the cellular uptake, intracellular delivery to lysosome, and reduction of stored substrates. Both enzymes were taken-up via endocytic pathway mediated by mannose and mannose-6-phosphate receptors and delivered to lysosomes. Noteworthy, rhHex-A diminished the levels of stored lipids and lysosome mass in fibroblasts from Tay-Sachs patients. Overall, these results confirm the potential of P. pastoris as host to produce recombinant ß-hexosaminidases intended to be used in the treatment of GM2 gangliosidosis.

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α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are the predominant mediators of glutamate-induced excitatory neurotransmission. It is widely accepted that AMPA receptors are critical for the generation and spread of epileptic seizure activity. Dysfunction of AMPA receptors as a causal factor in patients with intractable epilepsy results in neurotransmission failure. Brain-specific serine/threonine-protein kinase 1 (SAD-B), a serine-threonine kinase specifically expressed in the brain, has been shown to regulate AMPA receptor-mediated neurotransmission through a presynaptic mechanism. In cultured rat hippocampal neurons, the overexpression of SAD-B significantly increases the frequency of miniature excitatory postsynaptic currents (mEPSCs). Here, we showed that SAD-B downregulation exerted antiepileptic activity by regulating AMPA receptors in patients with temporal lobe epilepsy (TLE) and in the pentylenetetrazol (PTZ)-induced epileptic model. We first used immunoblotting and immunohistochemistry analysis to demonstrate that SAD-B expression was increased in the epileptic rat brain. Subsequently, to explore the function of SAD-B in epilepsy, we used siRNA to knock down SAD-B protein and observed behavior after PTZ-induced seizures. We found that SAD-B downregulation attenuated seizure severity and susceptibility in the PTZ-induced epileptic model. Furthermore, we showed that the antiepileptic effect of SAD-B downregulation on PTZ-induced seizure was abolished by CNQX (an AMPA receptor inhibitor), suggesting that SAD-B modulated epileptic seizure by regulating AMPA receptors in the brain. Taken together, these findings suggest that SAD-B may be a potential and novel therapeutic target to limit epileptic seizures.

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Many researchers have shown that pretreatment plasma fibrinogen levels are closely correlated with the prognosis of patients with lung cancer (LC). In this study, we thus performed a meta-analysis to systematically assess the prognostic value of pretreatment plasma fibrinogen levels in LC patients. A computerized systematic search in PubMed, EMBASE, Web of Science and China National Knowledge Infrastructure (CNKI) was performed up to March 15, 2018. Studies with available data on the prognostic value of plasma fibrinogen in LC patients were eligible for inclusion. The pooled hazard ratios (HRs) and odd ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the correlation between pretreatment plasma fibrinogen levels and prognosis as well as clinicopathological characteristics. A total of 17 studies with 6,460 LC patients were included in this meta-analysis. A higher pretreatment plasma fibrinogen level was significantly associated with worse overall survival (OS) (HR: 1.57; 95% CI: 1.39-1.77; p=0.001), disease-free survival (DFS) (HR: 1.53; 95% CI: 1.33-1.76; p=0.003), and progression-free survival (PFS) (HR: 3.14; 95% CI: 2.15-4.59; p<0.001). Furthermore, our subgroup and sensitivity analyses demonstrated that the pooled HR for OS was robust and reliable. In addition, we also found that a higher fibrinogen level predicted advanced TNM stage (III-IV) (OR=2.18, 95% CI: 1.79-2.66; p<0.001) and a higher incidence of lymph node metastasis (OR=1.74, 95% CI: 1.44-2.10; p=0.02). Our study suggested that higher pretreatment plasma fibrinogen levels predict worse prognoses in LC patients.

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Many researchers have shown that pretreatment plasma fibrinogen levels are closely correlated with the prognosis of patients with lung cancer (LC). In this study, we thus performed a meta-analysis to systematically assess the prognostic value of pretreatment plasma fibrinogen levels in LC patients. A computerized systematic search in PubMed, EMBASE, Web of Science and China National Knowledge Infrastructure (CNKI) was performed up to March 15, 2018. Studies with available data on the prognostic value of plasma fibrinogen in LC patients were eligible for inclusion. The pooled hazard ratios (HRs) and odd ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the correlation between pretreatment plasma fibrinogen levels and prognosis as well as clinicopathological characteristics. A total of 17 studies with 6,460 LC patients were included in this meta-analysis. A higher pretreatment plasma fibrinogen level was significantly associated with worse overall survival (OS) (HR: 1.57; 95% CI: 1.39-1.77; p=0.001), disease-free survival (DFS) (HR: 1.53; 95% CI: 1.33-1.76; p=0.003), and progression-free survival (PFS) (HR: 3.14; 95% CI: 2.15-4.59; p<0.001). Furthermore, our subgroup and sensitivity analyses demonstrated that the pooled HR for OS was robust and reliable. In addition, we also found that a higher fibrinogen level predicted advanced TNM stage (III-IV) (OR=2.18, 95% CI: 1.79-2.66; p<0.001) and a higher incidence of lymph node metastasis (OR=1.74, 95% CI: 1.44-2.10; p=0.02). Our study suggested that higher pretreatment plasma fibrinogen levels predict worse prognoses in LC patients.

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α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are the predominant mediators of glutamate-induced excitatory neurotransmission. It is widely accepted that AMPA receptors are critical for the generation and spread of epileptic seizure activity. Dysfunction of AMPA receptors as a causal factor in patients with intractable epilepsy results in neurotransmission failure. Brain-specific serine/threonine-protein kinase 1 (SAD-B), a serine-threonine kinase specifically expressed in the brain, has been shown to regulate AMPA receptor-mediated neurotransmission through a presynaptic mechanism. In cultured rat hippocampal neurons, the overexpression of SAD-B significantly increases the frequency of miniature excitatory postsynaptic currents (mEPSCs). Here, we showed that SAD-B downregulation exerted antiepileptic activity by regulating AMPA receptors in patients with temporal lobe epilepsy (TLE) and in the pentylenetetrazol (PTZ)-induced epileptic model. We first used immunoblotting and immunohistochemistry analysis to demonstrate that SAD-B expression was increased in the epileptic rat brain. Subsequently, to explore the function of SAD-B in epilepsy, we used siRNA to knock down SAD-B protein and observed behavior after PTZ-induced seizures. We found that SAD-B downregulation attenuated seizure severity and susceptibility in the PTZ-induced epileptic model. Furthermore, we showed that the antiepileptic effect of SAD-B downregulation on PTZ-induced seizure was abolished by CNQX (an AMPA receptor inhibitor), suggesting that SAD-B modulated epileptic seizure by regulating AMPA receptors in the brain. Taken together, these findings suggest that SAD-B may be a potential and novel therapeutic target to limit epileptic seizures.

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Desmodium caudatum (Thunb.) DC, is an ever-green plant widely used in the central and southern China with great economic value for their medical values on fever, dysentery, gastroenteritis, rectal prolapse, snake bites, mastitis, and boils carbuncle. Despite its extensive uses as a traditional Chinese medicine, no systematic research on the identification of Desmodium caudatum has been reported. In this study, traditional pharmacognostical identification including the botanical origin and morphological characters, medicinal material characters, microscopic characters, physicochemical parameters determination and phytochemical screening, and DNA barcoding analysis were employed to establish an accurate and effective identification system of Desmodium caudatum. In addition, the molecular pharmacognosy study was adopted in order to identify the samples more accurately. The ITS loci of the nuclear genome and psbA-trnH loci of the chloroplast genome were selected and evaluated, which were the most variable loci. The study will be beneficial to the development of the quality standard and the identification of species.

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Microbiome plays a key role in determining soil suppressiveness against invading pathogens. Our previous study revealed that microbial community of bulk soil could be manipulated by lime and ammonium bicarbonate fumigation followed by biofertilizer application. However, the assembly of microbial community suppressive to banana Panama disease in the rhizosphere is still unclear. In this study, we used high-throughput sequencing and quantitative PCR to explore the assembly of rhizosphere microbiome associated with banana Panama disease suppression in a two-seasonal pot experiment. We found biofertilizer applied to lime and ammonium bicarbonate fumigated soil significantly (P < 0.05) reduced the abundance of rhizosphere Fusarium oxysporum compared to biofertilizer applied to non-fumigated soil. Principal coordinate analysis revealed that biofertilizer applied to lime and ammonium bicarbonate fumigated soil re-shaped the rhizosphere bacterial community composition by increasing the phylogenetic relatedness, and stimulating indigenous microbes, for example, Gemmatimonas, Sphingomonas, Pseudomonas, Lysobacter and Bacillus. Co-occurrence analysis revealed that potential species involved in disease suppression were more interrelated in disease-suppressive soils. Taken together, lime and ammonium bicarbonate fumigation followed by biofertilizer application could induce banana rhizosphere to assemble beneficial microbes dominated consortia to suppress banana Panama disease.

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Abstract Various traditional systems of medicine enlightened the importance of Premna microphylla Turcz., Lamiaceae, medicinally. The present study was carried out to provide a scientific basis of the identification and the authenticity of P. microphylla with the help of pharmacognostical parameters, which is not done before. Roots, stems, and leaves of P. microphylla were collected for pharmacognostical studies involving macros, microscopic evaluation, physicochemical parameters analysis like fluorescence analysis and thin layer chromatography, in addition with DNA barcodes of internal transcribed spacer and psbA-trnH regions. Transverse section of root indicated the presence of stone cell bands. Transverse section of stem showed the presence of stone cells and vessels. Transverse section of leaf midrib revealed the presence of shaft type of porosity. Microscopic studies of powder revealed the presence of cork cells, fibers, vessels, nonglandular hairs, stone cells and glandular scale cells. Thin layer chromatography of the extract revealed the presence of oleanolic acid in P. microphylla with specific R f values. Identification through DNA barcode showed the sequence of internal transcribed spacer region was novel while the sequence of psbA-trnH region displayed no differences from known sequence. The observations confirmed that P. microphylla has an obvious pharmacognostical characteristics, which will be useful toward providing a reliable basis for identification, purity, quality and classification of the plant.

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SUMMARY: The experiment was conducted to evaluate the effects of dietary supplemental chromium (Cr) on growth performance, meat quality, intestinal morphology, mucosa Hsp70 mRNA expression and antioxidant status of ducks reared under heat stress conditions. All ducks were randomly divided into three treatment groups, respectively, control group (Control, 23 ± 2 °C), heat stress group (HS, 32 ±2 °C), Cr picolinate group (CrPic, 32 ± 2 °C, 0.2 mg Cr/kg). Feed and distilled-deionized water were available ad libitum for an experimental phase of 35 days. Samples were collected on the day 14, 21 and 35 to determine biological and hematological values. Results showed that heat stress or dietary supplemental Cr both didn't have distinct influence on growth performance (P>0.05), compared to controls. Ducks fed 0.2 mg Cr/kg diet had greater ultimate pH (pHu)(P<0.05) than HS group. At day 14, the ratio of villus height to crypt depth (V/C) in CrPic group significantly increased (P<0.05) than that of HS group in jejunum. Heat stress remarkably increased Hsp70 mRNA expression in jejunum compared with controls (P<0.05). While the expression of Hsp70 mRNA in CrPic group was significantly decreased compared with HS (P<0.05). At day 21, the V/C of ileum in CrPic group significantly increased compared with HS group (P<0.05). Serum SOD levels in CrPic group were significantly higher than those in HS group (P<0.05). At day 35, Hsp70 mRNA expression and serum T-SOD levels in CrPic group significantly increased compared with controls (P<0.05). T-AOC in HS group significantly decreased compared with controls (P<0.05). Results indicate that dietary Cr supplementation doesn't influence ducks' growth performance, but has a positive effect on meat quality, small intestine morphology, also regulates Hsp70 mRNA expression under heat stress conditions, and enhances the antioxidant status.

RESUMEN: Se evaluó los efectos del cromo (Cr) dietético suplementario sobre el rendimiento del crecimiento, la calidad de la carne, la morfología intestinal, la expresión del ARNm Hsp70 en la mucosa y el estado antioxidante de los patos criados bajo condiciones de estrés por calor. Todos los patos se dividieron aleatoriamente en tres grupos: grupo control (control, 23 ± 2 °C), grupo de estrés térmico (HS, 32 ± 2 °C) y grupo de picolinato de Cr (CrPic, 32 ± 2 °C, 0,2 mg Cr / kg). El alimento y el agua desionizada destilada estuvieron disponibles ad libitum durante la fase experimental de 35 días. Las muestras se recogieron los días 14, 21 y 35 para determinar los valores biológicos y hematológicos. Los resultados mostraron que el estrés térmico o la suplementación dietética de Cr no tuvieron una influencia distinta en el rendimiento del crecimiento (P> 0,05), en comparación con los controles. Los patos alimentados con 0,2 mg de Cr / kg de dieta tuvieron un mayor pH final (pHu) (P <0,05) que el grupo HS. En el día 14, la relación de la altura de las vellosidades a la profundidad de la cripta (V / C) en el grupo CrPic aumentó significativamente (P <0,05) en relación a la del grupo de HS en el yeyuno. El estrés por calor incrementó notablemente la expresión del ARNm de Hsp70 en el yeyuno en comparación con los controles (P <0,05). Mientras que la expresión del ARNm de Hsp70 en el grupo CrPic se redujo significativamente en comparación con HS (P <0,05). En el día 21, la relación V / C del íleon en el grupo CrPic aumentó significativamente en comparación con el grupo HS (p <0,05). Los niveles séricos de SOD en el grupo CrPic fueron significativamente más altos que los del grupo HS (P <0,05). En el día 35, la expresión de ARNm de Hsp70 y los niveles séricos de T-SOD en el grupo CrPic aumentaron significativamente en comparación con los controles (P <0,05). T-AOC en el grupo HS disminuyó significativamente en comparación con los controles (P <0,05). Los resultados indican que la suplementación dietética de Cr no influye en el rendimiento de crecimiento de los patos, pero tiene un efecto positivo en la calidad de la carne, en la morfología del intestino delgado, y también regula la expresión de ARNm de Hsp70 en condiciones de estrés calórico y mejora el estado antioxidante.

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BACKGROUND: Familial progressive hyper- and hypopigmentation (FPHH) is a rare genodermatosis that is characterized by diffuse hyper- and hypopigmented spots on the skin and mucous membranes. It is caused by a pathogenic mutation of the KITLG gene. OBJECTIVES: To investigate the clinical features and mutation of the KITLG gene in a Chinese family with FPHH. METHODS: Histopathological and immunohistochemical analysis of lesions from the proband was performed. The KITLG gene was screened for the presence of mutations. RESULTS: A Chinese family containing 14 individuals with FPHH was described, and the proband was a 5-year-old girl showing diffuse hyper- and hypopigmented lesions on her extremities and trunk. Histopathological and immunohistochemical staining for S100 and HMB45 of skin biopsy specimens from the hyperpigmented areas showed a striking increase in melanin throughout the epidermis, especially in the basal cell layer, and staining of hypopigmented area specimens displayed lower levels of melanin in the epidermis. Mutation analysis of the KITLG gene was performed, but no mutation was found. STUDY LIMITATIONS: The new pathogenic gene was not found. CONCLUSION: A family with FPHH was described. Analysis revealed that its members did not have any mutations of the KITLG gene, which provided evidence for genetic heterogeneity of this genodermatosis.

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Abstract Background: Familial progressive hyper- and hypopigmentation (FPHH) is a rare genodermatosis that is characterized by diffuse hyper- and hypopigmented spots on the skin and mucous membranes. It is caused by a pathogenic mutation of the KITLG gene. Objectives: To investigate the clinical features and mutation of the KITLG gene in a Chinese family with FPHH. Methods: Histopathological and immunohistochemical analysis of lesions from the proband was performed. The KITLG gene was screened for the presence of mutations. Results: A Chinese family containing 14 individuals with FPHH was described, and the proband was a 5-year-old girl showing diffuse hyper- and hypopigmented lesions on her extremities and trunk. Histopathological and immunohistochemical staining for S100 and HMB45 of skin biopsy specimens from the hyperpigmented areas showed a striking increase in melanin throughout the epidermis, especially in the basal cell layer, and staining of hypopigmented area specimens displayed lower levels of melanin in the epidermis. Mutation analysis of the KITLG gene was performed, but no mutation was found. Study limitations: The new pathogenic gene was not found. Conclusion: A family with FPHH was described. Analysis revealed that its members did not have any mutations of the KITLG gene, which provided evidence for genetic heterogeneity of this genodermatosis.

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Renal ischemia-reperfusion (I/R) injury ranks as the primary cause of acute renal injury with severe morbidity and mortality. Side population (SP) cells have recently drawn increasing attention due to their critical role in injury repair and regeneration. Unfortunately, the underlying mechanism involved in renal I/R remains poorly elucidated. Here, pronounced increases of stromal cell-derived factor-1 (SDF-1) and its receptor CXC chemokine receptor 4 (CXCR4) were substantiated in I/R kidneys from C57BL/6 mice subjected to clamp the bilateral renal pedicles to mimic renal ischemia. Similar up-regulation of them was also determined in SP cells upon simulated ischemia/reperfusion (SI/R). In contrast to non-SP cells, SP cells exhibited higher viability, apoptosis resistance, chemotaxis, and paracrine actions following SI/R treatment, and these were further enhanced after SDF-1 stimulation. Interestingly, blocking CXCR4 signaling with AMD3100 notably ameliorated the above effects. Mechanism analysis corroborated that SDF-1/CXCR4 further induced the expression of ATP-binding cassette transporter ABCG2, an essential element for SP-mediated kidney regeneration after renal I/R injury. Moreover, AMD3100 pretreatment strikingly attenuated ABCG2 elevation in SP cells. Additionally, sonic hedgehog (SHH)-Gli 1 signaling was involved in SDF-1/CXCR4-mediated ABCG2 expression. When SP cells pretreated with AMD3100 were intravenously injected into I/R mice, SP cell-mediated decreases in blood urea nitrogen, serum creatinine, and histological score of kidney were noticeably attenuated, indicating that blocking CXCR4 pathway mitigated the therapeutic function of SP cells in renal I/R injury. Together, this research suggests that SDF-1/CXCR4 axis might act, via Shh-Gli1-ABCG2 signaling, as a positive regulator of SP cell-based therapies for renal I/R by Shh-Gli 1-ABCG2 signaling.

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Panama disease caused by Fusarium oxysporum f. sp. cubense infection on banana is devastating banana plantations worldwide. Biological control has been proposed to suppress Panama disease, though the stability and survival of bio-control microorganisms in field setting is largely unknown. In order to develop a bio-control strategy for this disease, 16S rRNA gene sequencing was used to assess the microbial community of a disease-suppressive soil. Bacillus was identified as the dominant bacterial group in the suppressive soil. For this reason, B. amyloliquefaciens NJN-6 isolated from the suppressive soil was selected as a potential bio-control agent. A bioorganic fertilizer (BIO), formulated by combining this isolate with compost, was applied in nursery pots to assess the bio-control of Panama disease. Results showed that BIO significantly decreased disease incidence by 68.5%, resulting in a doubled yield. Moreover, bacterial community structure was significantly correlated to disease incidence and yield and Bacillus colonization was negatively correlated with pathogen abundance and disease incidence, but positively correlated to yield. In total, the application of BIO altered the rhizo-bacterial community by establishing beneficial strains that dominated the microbial community and decreased pathogen colonization in the banana rhizosphere, which plays an important role in the management of Panama disease.

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INTRODUCTION: Solitary fibrous tumors are mesenchymally derived masses most commonly originating from the lung pleura. CASE REPORT: Herein, we report a 6-month-old presenting with syndrome of inappropriate antidiuretic hormone secretion (SIADH) and a suprasellar mass. The mass proved to be a solitary fibrous tumor. This case and salient literature are reviewed. CONCLUSIONS: To our knowledge, this is the youngest patient to be described with a mass of this type within the central nervous system.

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Philadelphia chromosome positive (Ph+) acute lymphoblastic leukemia (ALL) cells are insensitive to BCR-ABL tyrosine kinase inhibitor imatinib, the underlying mechanisms remain largely unknown. Here, we showed that imatinib treatment induced significant upregulation of miR-21 and downregulation of PTEN in Ph+ ALL cell line Sup-b15. Transient inhibition of miR-21 resulted in increased apoptosis, PTEN upregulation and AKT dephosphorylation, whereas ectopic overexpression of miR-21 further conferred imatinib resistance. Furthermore, knockdown of PTEN protected the cells from imatinib-induced apoptosis achieved by inhibition of miR-21. Additionally, PI3K inhibitors also notably enhanced the effects of imatinib on Sup-b15 cells and primary Ph+ ALL cells similar to miR-21 inhibitor. Therefore, miR-21 contributes to imatinib resistance in Ph+ ALL cells and antagonizing miR-21 demonstrates therapeutic potential by sensitizing the malignancy to imatinib therapy.

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