scholarly journals Systemic and immunomodulatory effects of whole body therapeutic hypothermia

2011 ◽  
Vol 152 (15) ◽  
pp. 575-580 ◽  
Author(s):  
Vince Pongor ◽  
Gergely Toldi ◽  
Miklós Szabó ◽  
Barna Vásárhelyi

Several neurobiological mechanisms contribute to the development of ischemic-reperfusion damage of the central nervous system that may be modulated by hypothermia. Nowadays hypothermia is a therapeutic tool for the treatment of stroke and perinatal asphyxia. Hypothermia does not only affect the central nervous system, but also has systemic effects. It influences the muscular and cardiovascular system, the systematic metabolism, induces electrolyte changes, and decreases inflammation. This review summarizes the effects of therapeutic hypothermia on the immune system. Experiments on cell lines and in animals along with human experience indicate that short term (2-4 hours) hypothermia increases the levels of anti-inflammatory cytokines and decreases that of proinflammatory cytokines. Long term (>24 hours) hypothermia, however, increases proinflammatory cytokine levels. Furthermore, hypothermia inhibits lymphocyte proliferation and decreases HLA-DR expression associated with cell activation. These results suggest that therapeutic hypothermia has a systemic immunomodulatory effect. Further research is required to determine the contribution of immunomodulation to the defense of the central nervous system. Orv. Hetil., 2011, 152, 575–580.

2014 ◽  
Vol 20 (30) ◽  
pp. 97-100
Author(s):  
Хетагурова ◽  
Yuliana Khetagurova ◽  
Ревазова ◽  
Asya Revazova ◽  
Бораева ◽  
...  

Despite of significant progress in the development of technologies of clinical monitoring and the fetus and newborn pathology study, perinatal asphyxia or, more accurately – cerebral ischemia (CI) remain serious condition, causing significant mortality and long-term morbidity. Chi-acquired syndrome characterized by clinical and laboratory signs of acute brain injury due to asphyxia (ie, hypoxia, acidosis). The paper reflects the main clinical signs and neurosonographic lesion of the Central nervous system (CNS) in neonatal newborn infants with different gestational age who underwent CI mild to moderate severity.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi Wen ◽  
Nazila Salamat-Miller ◽  
Keethkumar Jain ◽  
Katherine Taylor

AbstractDirect delivery of therapeutic enzymes to the Central Nervous System requires stringent formulation design. Not only should the formulation design consider the delicate balance of existing ions, proteins, and osmolality in the cerebrospinal fluid, it must also provide long term efficacy and stability for the enzyme. One fundamental approach to this predicament is designing formulations with no buffering species. In this study, we report a high concentration, saline-based formulation for a human sulfatase for its delivery into the intrathecal space. A high concentration formulation (≤ 40 mg/mL) was developed through a series of systematic studies that demonstrated the feasibility of a self-buffered formulation for this molecule. The self-buffering capacity phenomenon was found to be a product of both the protein itself and potentially the residual phosphates associated with the protein. To date, the self-buffered formulation for this molecule has been stable for up to 4 years when stored at 5 ± 3 °C, with no changes either in the pH values or other quality attributes of the molecule. The high concentration self-buffered protein formulation was also observed to be stable when exposed to multiple freeze–thaw cycles and was robust during in-use and agitation studies.


Author(s):  
Audrey Rousseaud ◽  
Stephanie Moriceau ◽  
Mariana Ramos-Brossier ◽  
Franck Oury

AbstractReciprocal relationships between organs are essential to maintain whole body homeostasis. An exciting interplay between two apparently unrelated organs, the bone and the brain, has emerged recently. Indeed, it is now well established that the brain is a powerful regulator of skeletal homeostasis via a complex network of numerous players and pathways. In turn, bone via a bone-derived molecule, osteocalcin, appears as an important factor influencing the central nervous system by regulating brain development and several cognitive functions. In this paper we will discuss this complex and intimate relationship, as well as several pathologic conditions that may reinforce their potential interdependence.


2017 ◽  
Vol 84 (3) ◽  
pp. 353-356 ◽  
Author(s):  
Anna Rosati ◽  
Alessandra Cosi ◽  
Massimo Basile ◽  
Alice Brambilla ◽  
Renzo Guerrini ◽  
...  

Glia ◽  
2014 ◽  
Vol 62 (10) ◽  
pp. 1659-1670 ◽  
Author(s):  
Karelle Bénardais ◽  
Viktoria Gudi ◽  
Lijie Gai ◽  
Jasmin Neßler ◽  
Vikramjeet Singh ◽  
...  

1995 ◽  
Vol 268 (6) ◽  
pp. R1343-R1358 ◽  
Author(s):  
V. L. Brooks ◽  
J. W. Osborn

The importance of the sympathetic nervous system in short-term regulation of arterial pressure is well accepted. However, the question of whether neural systems participate in long-term control of pressure has been debated for decades and remains unresolved. The principal argument against such a control system is that arterial baroreceptors adapt to sustained changes in arterial pressure. In addition, denervation of baroreceptors has minimal to no effect on basal levels of arterial pressure chronically. This argument assumes, however, that baroreceptors provide the primary chronic feedback signal to the central nervous system. An alternate model is proposed in which circulating hormones, primarily arginine vasopressin and angiotensin II, provide a long-term afferent signal to the central nervous system via binding to specific receptors in central sites lacking a blood-brain barrier (circumventricular organs). Studies suggest that the release of the hormones and the sympathetic response to alterations in their plasma concentrations are nonadaptive but may be gated by baroreceptor input. Evidence that this "hormonal-sympathetic reflex" model may explain the long-term alterations in sympathetic activity in response to chronic salt depletion and salt loading as well as congestive heart failure is presented. Finally, the role of an impaired hormonal sympathetic reflex in hypertension, specifically salt-dependent hypertension, is discussed.


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