Reliability of Donor Lung Sampling in Lung Transplantation

Introduction: Ex vivo lung perfusion (EVLP) is a normothermic platform used to assess donor lungs. Many have studied biomarkers in lung injury, but it is unclear whether samples taken from one location are representative of the organ. Our objective was to investigate the uniformity of cytokine expression in tissue biopsies and in EVLP perfusates from various locations. Methods: In the tissue study, eight donor lungs were partitioned from apex to base. In each lung, three biopsies were taken from the third, sixth, and ninth slices, while two were taken from the lingula and an injury site. In the perfusate study, four samples were taken from four lobes in eight donors during EVLP. Expressions of IL-6, IL-8, IL-10, and IL-1β were measured using qPCR and ELISA. Results: In the tissue study, the mean intra-biopsy equal-variance F-value was 0.53. The median intra-biopsy coefficient of variation (CV) was 18%. In donors without gross focal injury, the mean comparisons of biopsies in each donor showed that the three consistent slices showed no differences and had a CV of 20%, which was similar to the intra-biopsy CV (p=0.80). Both the lingula and injury biopsies demonstrated larger differences from the rest. The median intra-lung CV of perfusates from different lobes was 4.9%. Conclusion: Intra-biopsy variances were consistent across biopsies. Lungs without gross focal injury demonstrated more consistent gene expression. The lingula is not a representative site due to high signal variability. The consistent measurements in EVLP perfusates provided a uniform picture of the inflammation.

Peran Ferritin pada Stroke Iskemik Akut

Stroke is a neurological deficit that occurs due to acute focal injury to the central nervous system that occurs solely due to vascular disorders, including cerebral infarction or bleeding. Ferritin is an intracellular and extracellular iron storage protein which is essential for iron homeostasis in the body. Ferritin is expressed in microglia and macrophages, and also in neurons. If there is cell damage due to ischemic stroke, ferritin will leave the cells and enter the serum. The hypoxia-ischemic state in stroke induces the expression of ferritin in oligodendrocytes and microglia. When there is oxidative stress, ferritin formation will increase. The function of ferritin in times of oxidative stress is still controversial. Ferritin in this condition can act as a scavenger and as a donor for free iron ions. Ischemic stroke patients with larger lesions and more severe neurological deficits showed higher serum ferritin levels and a higher likelihood of complications of bleeding transformation.

The Risk of Thrombotic Events in Anetoderma Affecting Young Patients

Anetoderma is a rare skin disease, and its associated risk of thromboembolic events is unknown. Anetoderma is characterized by focal injury of elastic fibers in the dermis, clinically expressed by atrophic skin lesions. We report the case of a young person with anetoderma, drawing attention to the risk of associated thromboembolic peril.

Pursuing the Need for Physical Activity in Recurrent CVA Patients During Hospitalization: A Case Report

Cerebrovascular accident (CVA) is a neurological deficit condition caused by an acute focal injury of the central nervous system by cerebral infarction or intracerebral hemorrhage. CVA patients who do not reduce risk factors after the first attack have an 8.7 times higher risk of CVA recurrence. The effect of a recurrent CVA is six times greater than the risk of a first CVA in the general population of the same age and sex, and nearly half of them remain alive but are physically disabled. This case report illustrates the process of recurrent CVA and disability experienced by a 69-year-old Malay woman, a patient at a private hospital in West Kalimantan. The nursing strategy of two post-CVA physical rehabilitation exercise programs for patients during hospitalization will be explained according to the stages in nursing theory.Abstrak Mengejar Kebutuhan Aktivitas Fisik Pasien CVA Berulang Selama Hospitalisasi: Laporan Kasus. Cerebrovaskuler Accident (CVA) adalah kondisi defisit neurologis karena cedera akut pada sistem saraf pusat disebabkan infark serebral atau perdarahan intraserebral. Pasien CVA yang tidak menurunkan faktor risikonya secara optimal setelah serangan pertama memiliki risiko CVA berulang sebesar 8,7 kali lebih tinggi. Efek dari CVA berulang adalah 6 kali lebih besar dari episode CVA pertama pada populasi umum, dengan usia dan jenis kelamin yang sama, hampir setengah dari mereka tetap hidup tetapi mengalami cacat secara fisik. Laporan kasus ini menggambarkan penyakit CVA berulang dan kecacatan yang dialami seorang wanita Melayu berusia 69 tahun, seorang pasien di Rumah Sakit Swasta, Kalimantan Barat. Strategi keperawatan untuk dua program latihan rehabilitasi fisik pasca-CVA bagi pasien selama hospitalisasi akan dijelaskan sesuai dengan tahapan pada teori keperawatan. Kata Kunci: aktivitas fisik, CVA berulang, hospitalisasi

Notch signaling via Hey1 and Id2b regulates Müller glia’s regenerative response to retinal injury

Unlike mammals, zebrafish can regenerate a damaged retina. Key to this regenerative response are Müller glia (MG) that divide and produce progenitors for retinal repair. Although factors regulating MG’s decision to divide remain mostly unknown, a certain threshold of neuron death must be exceeded in order for MG to engage in a regenerative response. A role for Notch signaling in this process is indicated since its inhibition expands the zone of injury-responsive MG following a focal injury. Our data show that injury-dependent changes in Dll4 and Dlb control Notch signaling in MG and that Hey1 and Id2b are downstream effectors that regulate proliferation of MG and MG-derived progenitors. Although we find Hey1 and Id2b can inhibit proliferation of MG-derived progenitors, only Hey1 is able to regulate MG’s injury response threshold. Remarkably, Hey1 suppression is sufficient to recapitulate the effects of Notch inhibition on MG’s injury response threshold.

EVALUATION OF LIPID PROFILE IN YOUNG ADULT STROKE PATIENT AT M Y HOSPITAL INDORE, MADHYA PRADESH

Introduction: Stroke is classically characterized as a neurological decit attributed to an acute focal injury of the central nervous system due to impairment of cerebral circulation, resulting in abnormal perfusion of brain causing acute neurological decit. Diabetes mellitus and dyslipidaemia, along with hypertension and smoking are the leading risk factors for the occurrence of stroke. It is most common in elderly patients, but stroke can occur at any age, including childhood. There are many risk factors found to be associated with the stroke but role of lipid abnormality as major risk factor is consistently observed. Aim & Objectives: To evaluate lipid prole status in young patients suffering from stroke and its relationship with etiology of stroke. Material & Methods: This prospective clinical study was conducted in M Y Hospital, Indore in the young (15-45 years) patients suffering from stroke attended the medicine department. The total50 patients were included in the study after informed consent. Complete lipid prole was evaluated using serum sample of patients by standard enzymatic methods in the central lab of hospital. Results & Observations: Total cholesterol, Triglycerides, HDL, LDL were found abnormal in 28,16%,82%,62% subjects presented with stroke. Out of theses patients presented with abnormal lipid status the percentage of ischaemic stroke was 13%,7%,32%,27% respectively and haemorrhagic stroke was observed in 01%, 01%,09%, 04% respectively. Conclusions: Our study concluded that relation of dyslipidaemia with ischaemic and haemorrhagic stroke patients isn't consistent and more related to ischaemic stroke as compared to haemorrhagic stroke.

Pursuing the Need for Physical Activity in Recurrent CVA Patients During Hospitalization: A Case Report

Cerebrovascular accident (CVA) is neurological deficit condition caused by an acute focal injury of the central nervous system by cerebral infarction or intracerebral hemorrhage. CVA patients who do not reduce risk factors after the first attack have an 8.7 times higher risk of CVA recurrence. The effect of a recurrent CVA is six times greater than the risk of a first CVA in the general population of the same age and sex, and nearly half of them remain alive but are physically disabled. This case report illustrates the process of recurrent CVA and disability experienced by a 69-year-old Malay woman, a patient at a private hospital in West Kalimantan. The nursing strategy of two post-CVA physical rehabilitation exercise programs for patients during hospitalization will be explained according to the stages in nursing theory. Abstrak Mengejar Kebutuhan Aktivitas Fisik pada Pasien CVA Berulang Selama Hospitalisasi: Laporan Kasus. Cerebrovaskuler Accident (CVA) adalah kondisi sebagai defisit neurologis karena cedera akut pada sistem saraf pusat disebabkan infark serebral atau perdarahan intraserebral. Pasien CVA yang tidak menurunkan faktor risikonya secara optimal setelah serangan pertama memiliki risiko CVA berulang sebesar 8,7 kali lebih tinggi. Efek dari CVA berulang adalah 6 kali lebih besar dari episode CVA pertama pada populasi umum, usia dan jenis kelamin yang sama, hampir setengah dari mereka tetap hidup tetapi mengalami cacat secara fisik. Laporan kasus ini menggambarkan gambaran penyakit CVA berulang dan kecacatan yang dialami seorang wanita Melayu berusia 69 tahun, seorang pasien di Rumah Sakit Swasta, Kalimantan Barat. Strategi keperawatan untuk dua program latihan rehabilitasi fisik pasca-CVA bagi pasien selama hospitalisasi akan dijelaskan sesuai dengan tahapan pada teori keperawatan. Kata Kunci: aktivitas fisik, recurrent cerebrovascular accident, hospitalisasi

Intravenous sulforhodamine B reduces alveolar surface tension, improves oxygenation and reduces ventilation injury in a respiratory distress model

In the neonatal (NRDS) and acute (ARDS) respiratory distress syndromes, mechanical ventilation supports gas exchange but can cause ventilation-induced lung injury (VILI) that contributes to high mortality. Further, surface tension, T, should be elevated and VILI is proportional to T. Surfactant therapy is effective in NRDS but not ARDS. Sulforhodamine B (SRB) is a potential alternative T-lowering therapeutic. In anesthetized male rats, we injure the lungs with 15 min of 42 ml/kg tidal volume, VT, and zero end-expiratory pressure ventilation. Then, over 4 hrs, we support the rats with protective ventilation - VT of 6 ml/kg with positive end-expiratory pressure. At the start of the support period, we administer intravenous non-T­-altering fluorescein (targeting 27 mM in plasma) without or with therapeutic SRB (10 nM). Throughout the support period, we increase inspired oxygen fraction, as necessary, to maintain >90% arterial oxygen saturation. At the end of the support period we sacrifice the rat; sample systemic venous blood for injury marker ELISAs; excise the lungs; combine confocal microscopy and servo-nulling pressure measurement to determine T in situ in the lungs; image fluorescein in alveolar liquid to assess local permeability; and determine lavage protein content and wet-to-dry ratio (W/D), both to assess global permeability. Lungs exhibit focal injury. Surface tension is elevated 72% throughout control lungs and in uninjured regions of SRB-treated lungs, but normal in injured regions of treated lungs. Sulforhodamine B administration improves oxygenation, reduces W/D and reduces plasma injury markers. Intravenous SRB holds promise as a therapy for respiratory distress.

Local sleep-like cortical reactivity in the awake brain after focal injury

The functional consequences of focal brain injury are thought to be contingent on neuronal alterations extending beyond the area of structural damage. This phenomenon, also known as diaschisis, has clinical and metabolic correlates but lacks a clear electrophysiological counterpart, except for the long-standing evidence of a relative EEG slowing over the injured hemisphere. Here, we aim at testing whether this EEG slowing is linked to the pathological intrusion of sleep-like cortical dynamics within an awake brain. We used a combination of transcranial magnetic stimulation and electroencephalography (TMS/EEG) to study cortical reactivity in a cohort of 30 conscious awake patients with chronic focal and multifocal brain injuries of ischaemic, haemorrhagic and traumatic aetiology. We found that different patterns of cortical reactivity typically associated with different brain states (coma, sleep, wakefulness) can coexist within the same brain. Specifically, we detected the occurrence of prominent sleep-like TMS-evoked slow waves and off-periods—reflecting transient suppressions of neuronal activity—in the area surrounding focal cortical injuries. These perilesional sleep-like responses were associated with a local disruption of signal complexity whereas complex responses typical of the awake brain were present when stimulating the contralesional hemisphere. These results shed light on the electrophysiological properties of the tissue surrounding focal brain injuries in humans. Perilesional sleep-like off-periods can disrupt network activity but are potentially reversible, thus representing a principled read-out for the neurophysiological assessment of stroke patients, as well as an interesting target for rehabilitation.

Splitting up to heal: mitochondrial shape regulates signaling for focal membrane repair

Mitochondria are central to the health of eukaryotic cells. While commonly known for their bioenergetic role, mitochondria also function as signaling organelles that regulate cell stress responses capable of restoring homeostasis or leading the stressed cell to eventual death. Damage to the plasma membrane is a potentially fatal stressor incurred by all cells. Repairing plasma membrane damage requires cells to mount a rapid and localized response to injury. Accumulating evidence has identified a role for mitochondria as an important facilitator of this acute and localized repair response. However, as mitochondria are organized in a cell-wide, interconnected network, it is unclear how they collectively sense and respond to a focal injury. Here we will discuss how mitochondrial shape change is an integral part of this localized repair response. Mitochondrial fragmentation spatially restricts beneficial repair signaling, enabling a localized response to focal injury. Conservation of mitochondrial fragmentation in response to cell and tissue damage across species demonstrates that this is a universal pro-survival adaptation to injury and suggests that mitochondrial fragmentation may provide cells a mechanism to facilitate localized signaling in contexts beyond repairing plasma membrane injury.