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Dorsal mesencephalic modulation of breathing and autonomic outflow.

Elements in the medullary ventral respiratory column nuclei and dorsal respiratory group interact with the Kölliker-Fuse and medial parabrachial nuclei to generate the breathing rhythm and pattern. Triphasic eupnea consists of inspiratory [I], post-inspiratory [post-I], and late-expiratory [E2] phases. Mesencephalic zones exert modulatory influences upon respiratory rhythm generating circuitry, sympathetic oscillators, and parasympathetic nuclei. The earliest evidence supporting this derives from studies performed by Martin and Booker in 1878. These authors demonstrated augmentation of ventilation in response to electrical stimulation of the mesencephalic colliculi in the rabbit. A series of studies performed during the past several decades revealed a critical contribution of the red nucleus in mediating hypoxic ventilatory depression. Stimulation of distributed zones within the midbrain elicited seemingly disparate effects upon respiratory phase timing and transitioning. The works of Schmid and Böhmer demonstrated monosynaptic modulation of medullary inspiratory and expiratory related units in response to stimulation within midbrain zones corresponding with the red nucleus and rubrospinal tract. A plethora of studies have since generated strong evidence demonstrating and underscoring a critical contribution of the mesencephalic colliculi and periaqueductal gray matter in coordinately amplifying the respiratory output and sympathetic tone, blunting the Hering Breuer reflex and barosensitivity, and generating defense reaction behavioral responses to imminent environmental dangers. The lateral and ventrolateral divisions of the periaqueductal gray matter play critical roles in coordinating vocalization with breathing in an integrated circuit with the parabrachial nuclei. Authors have critically highlighted extensive and specific locoregional heterogeneity of effects elicited from periaqueductal gray matter stimulation. Studies have also made significant strides into elucidating the mechanistic basis and monosynaptic and polysynaptic propriobulbar and bulbospinal circuitry mediating periaqueductal gray matter and collicular modulation of breathing and autonomic outflow. The periaqueductal gray matter thus modulates and shapes neural respiratory frequency and amplitude, respiratory phase transitions, and autonomic outflow and appropriately coordinates defense reaction behavioral responses. The data collectively inspire fruitful new avenues of investigation in order to more thoroughly elucidate the mechanistic underpinnings of coordinate effects of the mesencephalic periaqueductal gray matter modulating the cardiovascular and respiratory outputs. We discuss and review the literature evaluating the role of the periaqueductal gray matter in modulating the respiratory and cardiovascular outputs.

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SWI / SNF Nucleosome Complex-Deficient Colorectal Carcinomas Have Distinct Clinicopathologic Features.

The switch/sucrose-nonfermenting (SWI/SNF) nucleosome complex consists of several proteins that are involved in cellular proliferation and tumor suppression. The aim of this study was to correlate immunohistochemical expression of four SWI/SNF complex subunits, SMARCA2, SMARCB1, SMARCA4, and ARID1A, with clinicopathologic and molecular features and patient survival in 338 patients with colorectal adenocarcinoma using a tissue microarray approach. Twenty-three (7%) colorectal adenocarcinomas demonstrated deficient SWI/SNF expression: 7 had SMARCA2 deficiency, 12 had ARID1A deficiency, and 4 had both SMARCA2 and ARID1A deficiency. No cases were SMARCB1 or SMARCA4-deficient. Twelve (52%) SWI/SNF complex-deficient tumors demonstrated MMR deficiency (p=0.02), 6 (26%) showed medullary differentiation (p=0.001), and 9 were negative for CDX2 expression (p<0.001). Among the MMR deficient SWI/SNF complex-deficient tumors, 8 were sporadic MLH1 deficient and 4 were seen in Lynch syndrome patients. Compared to ARID1A-deficient alone tumors, SMARCA2-deficient tumors were less likely to exhibit MMR deficiency (27% vs. 75%, p=0.04), medullary differentiation (0% vs. 50%, p=0.01), and mucinous differentiation (0% vs. 42%, p=0.04). Conventional gland-forming histology was more often identified in SMARCA2-deficient tumors (11/11, 100%) compared to tumors with ARID1A deficiency alone (4/12, 33%) (p=0.001). There was no difference in KRAS mutation, BRAF mutation, stage, disease-specific survival, or disease-free survival for patients stratified by SWI/SNF expression (all with p>0.05). In conclusion, SMARCA2-deficient and ARID1A-deficient colorectal carcinomas had distinctly different clinicopathologic features with ARID1A-deficient tumors exhibiting medullary and mucinous differentiation and MMR deficiency, and SMARCA2-deficient tumors demonstrating conventional gland-forming histologic growth with less frequent MMR deficiency.

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Comment on "Which Factors Affect the Severity of Dysphagia in Lateral Medullary Infarction?"


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Intramedullary tibia nailing with external fixation.

This study introduces an intramedullary nailing technique with external fixation and aims to determine the safest position of Schanz screws for this technique.

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Effect of Lenvatinib on a Patient with Medullary Thyroid Carcinoma Liver Metastasis Caused by Multiple Endocrine Neoplasia Type 2A.

A 61-year-old female was diagnosed with multiple endocrine neoplasia type 2A (MEN2A), caused by a heterozygous point mutation in the RET gene (TGC to TAC at codon 634) resulting in the substitution of cytosine with leucine (C634Y). The patient had pheochromocytoma (PCC) in the left adrenal gland and medullary thyroid carcinoma (MTC) with liver metastasis. Primary hyperparathyroidism (PHP) was not evident. Family history data suggested that the RET gene mutation was inherited from the father. The PCC was removed laparoscopically, but the MTC was observed conservatively for 7 years because the status of the MTC was compatible with T1N1M1 and stage IVC; therefore, it was not curable with surgery. The MTC liver metastasis increased in size. Lenvatinib, an oral multi-tyrosine kinase inhibitor, was administered until the patient had received a total dose of 1336mg, and then administration was stopped because of nausea. The reduction rate of the MTC liver metastasis was 31%, which was considered partial response. At this point, the patient was doing well, suggesting that lenvatinib was effective in treating the MTC liver metastasis and may be one of the treatment for advanced MTC caused by C634Y mutation in the RET gene.

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Insulinoma-associated protein 1 (INSM1): a potential biomarker and therapeutic target for neuroendocrine tumors.

Insulinoma-associated protein 1 (INSM1), a transcriptional regulator with a zinc-finger DNA-binding domain, has been validated as a cytoplasmic marker for neuroendocrine differentiation of tumor cells. Next to its abundant expression in the fetal pancreas, it is expressed in brain tumors, pheochromocytomas, medullary thyroid carcinomas, insulinomas and pituitary and small-cell lung carcinomas. INSM1 is not expressed in normal adult tissues and/or most non-neuroendocrine tumors. It regulates various downstream signaling pathways, including the Sonic Hedgehog, PI3K/AKT, MEK/ERK1/2, ADK, p53, Wnt, histone acetylation, LSD1, cyclin D1, Ascl1 and N-Myc pathways. Although INSM1 appears to be a subtle and specific biomarker for neuroendocrine tumors, its role in tumor development has remained unclear.

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Expression of NaPi-IIb in rodent and human kidney and upregulation in a model of chronic kidney disease.

Na-coupled phosphate cotransporters from the SLC34 and SLC20 families of solute carriers mediate transepithelial transport of inorganic phosphate (Pi). NaPi-IIa/Slc34a1, NaPi-IIc/Slc34a3, and Pit-2/Slc20a2 are all expressed at the apical membrane of renal proximal tubules and therefore contribute to renal Pi reabsorption. Unlike NaPi-IIa and NaPi-IIc, which are rather kidney-specific, NaPi-IIb/Slc34a2 is expressed in several epithelial tissues, including the intestine, lung, testis, and mammary glands. Recently, the expression of NaPi-IIb was also reported in kidneys from rats fed on high Pi. Here, we systematically quantified the mRNA expression of SLC34 and SLC20 cotransporters in kidneys from mice, rats, and humans. In all three species, NaPi-IIa mRNA was by far the most abundant renal transcript. Low and comparable mRNA levels of the other four transporters, including NaPi-IIb, were detected in kidneys from rodents and humans. In mice, the renal expression of NaPi-IIa transcripts was restricted to the cortex, whereas NaPi-IIb mRNA was observed in medullary segments. Consistently, NaPi-IIb protein colocalized with uromodulin at the luminal membrane of thick ascending limbs of the loop of Henle segments. The abundance of NaPi-IIb transcripts in kidneys from mice was neither affected by dietary Pi, the absence of renal NaPi-IIc, nor the depletion of intestinal NaPi-IIb. In contrast, it was highly upregulated in a model of oxalate-induced kidney disease where all other SLC34 phosphate transporters were downregulated. Thus, NaPi-IIb may contribute to renal phosphate reabsorption, and its upregulation in kidney disease might promote hyperphosphatemia.

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Role of the renin-angiotensin system in kidney development and programming of adult blood pressure.

Adverse events during fetal life such as insufficient protein intake or elevated transfer of glucocorticoid to the fetus may impact cardiovascular and metabolic health later in adult life and are associated with increased incidence of type 2 diabetes, ischemic heart disease and hypertension. Several adverse factors converge and suppress the fetal renin-angiotensin-aldosterone system (RAAS). The aim of this review is to summarize data on the significance of RAAS for kidney development and adult hypertension. Genetic inactivation of RAAS in rodents at any step from angiotensinogen to angiotensin II (ANGII) type 1 receptor (AT1) receptors or pharmacologic inhibition leads to complex developmental injury to the kidneys that has also been observed in human case reports. Deletion of the 'protective' arm of RAAS, angiotensin converting enzyme (ACE) 2 (ACE-2) and G-protein coupled receptor for Angiotensin 1-7 (Mas) receptor does not reproduce the AT1 phenotype. The changes comprise fewer glomeruli, thinner cortex, dilated tubules, thicker arterioles and arteries, lack of vascular bundles, papillary atrophy, shorter capillary length and volume in cortex and medulla. Altered activity of systemic and local regulators of fetal-perinatal RAAS such as vitamin D and cyclooxygenase (COX)/prostaglandins are associated with similar injuries. ANGII-AT1 interaction drives podocyte and epithelial cell formation of vascular growth factors, notably vascular endothelial growth factor (VEGF) and angiopoietins (Angpts), which support late stages of glomerular and cortical capillary growth and medullary vascular bundle formation and patterning. RAAS-induced injury is associated with lower glomerular filtration rate (GFR), lower renal plasma flow, kidney fibrosis, up-regulation of sodium transporters, impaired sodium excretion and salt-sensitive hypertension. The renal component and salt sensitivity of programmed hypertension may impact dietary counseling and choice of pharmacological intervention to treat hypertension.

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