Increasing atmospheric temperature implicates increasing risk for acute type A dissection in hypertensive patients

Background: Acute type A aortic dissection (AAAD) is a life-threatening condition with high mortality within 24 hours. We hypothesized if there is a correlation between seasonal weather changes and the occurrence of AAAD. The aim of the present study was to identify seasonal specific weather and patient characteristics predicting the occurrence of AAAD. Methods: This is a retrospective analysis of all consecutive patients of our department with AAAD between January 1st 2006 and December 31st 2016. The national meteorological department provided the data of temperature, humidity and air pressure during the study period. The occurrence of AAAD, preoperative neurological impairment and mortality were analyzed in correlation with the obtained daily weather data within the entire cohort and in patients with and without hypertension separately. Results: A total of 517 patients were included. Mean age was 63.4±13 years, 69.4% were male and 68.8% had documented hypertension. In-hospital mortality was 17.7%. In the whole cohort, the occurrence of AAAD was significantly increased in March, October, December (P=0.016). In hypertensive patients, the occurrence was increased 34% with rising temperature (0.1-9.6 °C, OR1.34, 95% CI: 1.06-1.69, P=0.015). There was no correlation between weather variables and preoperative neurological impairment or mortality. Conclusions: Our data suggests a relation between an increasing number of events of AAAD and certain months within our catchment area and a significantly increased occurrence with rising temperatures (independent from absolute temperature at time of the event) in hypertensive patients

Survival, Neurologic Injury, and Kidney Function after Surgery for Acute Type A Aortic Dissection

Background To analyze survival, neurologic injury, and kidney function after acute type A aortic dissection. Methods A total of 445 patients undergoing surgery for acute type A aortic dissection were analyzed. Evaluation according to risk factors for mortality, neurologic injury, and kidney function was performed. Results Overall 1-, 5-, and 10-year survival rates were 82.8 ± 1.8%, 73.6 ± 2.4%, and 59.3 ± 3.9, respectively. Independent preoperative risk factors for mortality were preexisting renal impairment (p = 0.001), reduced left ventricular ejection fraction (p < 0.001), and age (p < 0.001). Perioperative risk factors were prolonged cross-clamp (p < 0.001) and cerebral perfusion time (p = 0.001). Risk factors for renal failure were preexisting renal impairment (p < 0.001), prolonged cross-clamp time (p < 0.001), cerebral perfusion time (p < 0.001), and age (p = 0.022). Risk factors for neurologic injury were cross-clamp time (p = 0.038), cerebral perfusion time (p = 0.007), and age (p = 0.045). Conclusion In addition to classic risk factors, survival after type A aortic dissection is affected by preexisting renal impairment. Preexisting renal impairment is predictive of postoperative renal failure. Therefore treatment and prevention strategies for renal failure during the acute and long-term course after acute type A aortic dissection are warranted

Cell Junction Pathology of Neural Stem Cells Is Associated With Ventricular Zone Disruption, Hydrocephalus, and Abnormal Neurogenesis

Fetal-onset hydrocephalus affects 1 to 3 per 1,000 live births. It is not only a disorder of cerebrospinal fluid dynamics but also a brain disorder that corrective surgery does not ameliorate. We hypothesized that cell junction abnormalities of neural stem cells (NSCs) lead to the inseparable phenomena of fetal-onset hydrocephalus and abnormal neurogenesis. We used bromodeoxyuridine labeling, immunocytochemistry, electron microscopy, and cell culture to study the telencephalon of hydrocephalic HTx rats and correlated our findings with those in human hydrocephalic and nonhydrocephalic human fetal brains (n = 12 each). Our results suggest that abnormal expression of the intercellular junction proteins N-cadherin and connexin-43 in NSC leads to 1) disruption of the ventricular and subventricular zones, loss of NSCs and neural progenitor cells; and 2) abnormalities in neurogenesis such as periventricular heterotopias and abnormal neuroblast migration. In HTx rats, the disrupted NSC and progenitor cells are shed into the cerebrospinal fluid and can be grown into neurospheres that display intercellular junction abnormalities similar to those of NSC of the disrupted ventricular zone; nevertheless, they maintain their potential for differentiating into neurons and glia. These NSCs can be used to investigate cellular and molecular mechanisms underlying this condition, thereby opening the avenue for stem cell therapy

Cell Junction Pathology of Neural Stem Cells Is Associated With Ventricular Zone Disruption, Hydrocephalus, and Abnormal Neurogenesis

Fetal-onset hydrocephalus affects 1 to 3 per 1,000 live births. It is not only a disorder of cerebrospinal fluid dynamics but also a brain disorder that corrective surgery does not ameliorate. We hypothesized that cell junction abnormalities of neural stem cells (NSCs) lead to the inseparable phenomena of fetal-onset hydrocephalus and abnormal neurogenesis. We used bromodeoxyuridine labeling, immunocytochemistry, electron microscopy, and cell culture to study the telencephalon of hydrocephalic HTx rats and correlated our findings with those in human hydrocephalic and nonhydrocephalic human fetal brains (n = 12 each). Our results suggest that abnormal expression of the intercellular junction proteins N-cadherin and connexin-43 in NSC leads to 1) disruption of the ventricular and subventricular zones, loss of NSCs and neural progenitor cells; and 2) abnormalities in neurogenesis such as periventricular heterotopias and abnormal neuroblast migration. In HTx rats, the disrupted NSC and progenitor cells are shed into the cerebrospinal fluid and can be grown into neurospheres that display intercellular junction abnormalities similar to those of NSC of the disrupted ventricular zone; nevertheless, they maintain their potential for differentiating into neurons and glia. These NSCs can be used to investigate cellular and molecular mechanisms underlying this condition, thereby opening the avenue for stem cell therapy

Guidelines for the use of flow cytometry and cell sorting in immunological studies

International audienceThe classical model of hematopoiesis established in the mouse postulates that lymphoid cells originate from a founder population of common lymphoid progenitors. Here, using a modeling approach in humanized mice, we showed that human lymphoid development stemmed from distinct populations of CD127(-) and CD127(+) early lymphoid progenitors (ELPs). Combining molecular analyses with in vitro and in vivo functional assays, we demonstrated that CD127(-) and CD127(+) ELPs emerged independently from lympho-mono-dendritic progenitors, responded differently to Notch1 signals, underwent divergent modes of lineage restriction, and displayed both common and specific differentiation potentials. Whereas CD127(-) ELPs comprised precursors of T cells, marginal zone B cells, and natural killer (NK) and innate lymphoid cells (ILCs), CD127(+) ELPs supported production of all NK cell, ILC, and B cell populations but lacked T potential. On the basis of these results, we propose a "two-family" model of human lymphoid development that differs from the prevailing model of hematopoiesis