Cardiac Intervention Before Liver Transplantation

BackgroundCardiovascular complication is one of the leading causes of mortality after liver transplantation (LT). Thus, a thorough cardiac evaluation is a must before proceeding to a liver transplant surgery. Percutaneous coronary intervention (PCI) with stent and to a lesser extent coronary artery bypass grafting (CABG) are both valuable treatment options for patients with coronary artery disease.MethodsA retrospective, single-center study that included patients who underwent cardiac intervention and subsequent LT for end-stage liver disease. All patients who had PCI or CABG were included in the study.ResultsTwenty-nine adult patients out of 51 had a cardiac intervention before liver transplantation. Twenty-four patients had a diagnostic PCI, 3 patients had therapeutic PCI with stent, and 2 had failed PCI and proceeded to CABG before liver transplant. The mean age of the patients was 60.5 years. There were 24 men. All patients had cirrhosis. The 2 CABG cases were done during the same admission with a 13- and 18-day interval between the CABG and the transplantation. Both cases were live-related liver transplantation. No mortality was reported.ConclusionIn case of PCI failure, CABG may be a valuable and safe treatment option for cirrhotic patients as a preparation for liver transplantation. Live donor liver transplantation may be a good back-up for those patients in case they develop hepatic decompensation.     

Synthesis of sulphonic acids and sultam derivatives

Reaction of propane-1,3-sultone with amines gave N-substituted aminosulphonic acids2a?i. Dehydration of2a?c with POCl₃ gave the corresponding sultams3a?c. Propane-1,3-sultone1 reacted with tertury amines to give the betaiene salts4–11. 2,4-Dimethyl-1,3-butadiene-1,4-sultone12 condensed with amines to give N-substituted-2,4-dimethyl-1,3-butadiene-1,4-sultams13a and13b. The reaction of3a, 13a with hydrazine hydrate gave acid hydrazides3d or13c. Compounds3d, 13c reacted with isocyanates to yield urea derivatives14a?c, 15a?c.     

High-dose treatment with lanreotide of patients with advanced neuroendocrine gastrointestinal tumors: Clinical and biological effects

Background: Neuroendocrine tumors usually present with inoperable metastatic disease and severe hormonal symtoms. Specific chemotherapy, alpha-interferon and the somatostatin analog octreotide are established therapies in these patients but all of them eventually fail. Other somatostatin analogs, e.g., RC-160 and lanreotide, are currently being studied in different doses and modes of administration.Patients and methods: Nineteen patients with advanced neuroendocrine gastrointestinal tumors [13 carcinoids and six endocrine pancreatic tumors (EPT)], liver metastases being present in 18, most of them heavily pretreated, were included. Seventeen out of 18 patients had somatostatin receptors demonstrated by octreotide scintigraphy. Lanreotide was given as four daily subcutaneous injections, starting with 750 µg/d, then increasing every week up to 12,000 µg/d after six weeks, a dose which was maintained, if tolerated, for 12 months, or until progression.Results: There was a significant tumor size response (>50%) in one patient (5%), whereas 12 patients (70%) had tumor stabilization for 12 months. Bichemical tumor markers were significantly reduced at six months (urinary 5-hydroxyindoleacetic acid and plasma chromogranin) and 12 months (chromogranin) and the overall biochemical response rate was 58% with this high dose of lanreotide. Adverse events were observed and four patients stopped the treatment due to adverse events. Studies of tumor biopsies before and during treatment indicated induction of apoptosis in patients with tumor stabilization and biochemical response.Conclusion: High-dose treatment with lanreotide (12,000 µg/d) produced tumor size response in 5%, stabilization in 70% and a biochemical response in 58% of patients. These results should be related to the advanced stage of the disease as indicated by the mean duration of disease of more than four years, but they do not appear to be better than those achieved with standard doses of somatostatin analogs. However, in responding patients we observed induction of apoptosis in the tumors, a phenomenon not seen with regular doses of somatostatin analogs, but often produced by chemotherapeutic agents.     

Effectiveness of an early mobility protocol for stroke patients in Intensive Care Unit

Objectives:To evaluate the effectiveness of an early mobility protocol for stroke patients in the intensive care unit.Methods:Participants were patients with first or recurrent stroke (n=60, age=49.02±6.36 years, body mass index=32.95±5.67 kg/m²) admitted to the intensive care stroke unit in general hospitals, Riyadh during October and December 2016. Single group pretest-posttest design involving an early mobility protocol was started within first 24 hours admission. Pre and post measurements of muscle strength, pulmonary function and quality of life were carried out.Results:There were significant improvements in muscle strength of upper and lower extremities´ muscles after treatment (p<0.05), pulmonary functions including Forced Vital Capacity, Forced Expiratory Volume 1 (p<0.05) and quality of life, namely, Barthel Index and modified Rankin Scale (p<0.01).Conclusion:This study demonstrates that initiating an early mobility protocol is safe and effective for intensive care unit stroke patients and supports introducing the current protocol as a standard protocol in neurogenic Intensive Care Units.

Stroke is a life-threatening condition caused by interruption of the blood supply to any part of the brain. Stroke causes acute neurological disorders and long-term disabilities and imposes economic, social and health impacts on individuals and their families.1 Survivors of stroke are left with mental and physical disabilities that cause social and economic burdens and impair quality of life (QOL). In Saudi Arabia stroke is becoming a rapidly increasing problem and a primary cause of morbidity and mortality.2 Worldwide the incidence of first-time stroke was 17 million during 1990-2000.3 Cerebrovascular diseases including stroke is a leading cause of mortality,4 and stroke is the fifth leading cause of death, but it remains the first cause of disability in the USA.5 By 2030 there will be almost 12 million stroke deaths and 70 million stroke survivors globally.6 Stroke has an adverse influence on the QOL of patients. The onset of stroke is sudden, and unlike other disabling conditions, it leaves patients and their family’s ill prepared for its sequelae.7 Stroke may create unique conditions that affect the patients’ QOL, involving dysfunctions in physical, emotional, memory, thinking, and social interactions.8Stroke is an urgent health care issue. It is a common cause of the hospital admissions. Immediate admission to the neuro-intensive care unit can facilitate early stroke treatment strategies.9 Stroke patients in the intensive care unit (ICU) experience a decrease in physical activity that represents a significant stress on the body and leads to a considerable decrease in functional status, increases morbidity, mortality rate, and duration of hospital stay and cost of care.10 In addition to comorbid diseases, patients on mechanical ventilation have many barriers to mobility because they are surrounded by tubes, catheters, life support and monitoring equipment. Additionally, other factors besides weakness, such as sleep loss, lack of social communication, nutritional status, sedation, and an ICU culture that encourages bed rest further contribute to functional deterioration.11 There is considerable loss of the muscle mass during the initial weeks of immobility in the ICU, therefore its management is inherently related to QOL after discharge.12 Considerable published evidence indicates that patients in ICUs have high morbidity and mortality, high costs of care and a marked decline in functional status.13,14Early and progressive mobilization program has been described as a key component for patients in the ICU. It may decrease post stroke complications such as infections, deep venous thrombosis, pneumonia, pressure ulcers, falls and de-conditioning with bed rest.15 It has been recognized that mobilization of post stroke patients is essential to prevent hospital-associated complications, functional decline and facilitate recovery.16 Moreover, the benefits of early mobilization include decreased ICU-acquired weakness, improved functional recovery within hospital,17 Effective stroke intervention begins the day the patient has a stroke.18 It has a positive effect on patient functional ability, promotes positive psychological effects and improves walking at hospital discharge and reduces hospital length of stay.19 While on the other hand, long term inactivity may affect the patients’ physical, social, emotional, behavioral, and psychological pattern.20 In addition, secondary changes associated with stroke-related inactivity include muscle atrophy, a shift in muscle fiber type to a greater predominance of fast-fatigable, insulin-resistant fibers, loss of cardiovascular fitness, and increased intramuscular fat.21 Therefore, early mobilization program which is a complex intervention that needs crucial patient assessment and management, as well as interdisciplinary team collaboration and training.22,23 The early mobilization may improve patient outcomes and recovery.24 Few studies have investigated the role of increased mobility in ICU patients. Therefore, this prospective intervention trial evaluated the effectiveness of an early mobility program administered by physical therapists and nursing personnel for stroke patients admitted in ICU.     

Estrogen activates mitogen-activated protein kinase in native, nontransfected CHO-K1, COS-7, and RAT2 fibroblast cell lines

CHO-K1, COS-7, and Rat2 fibroblast cell lines are generally believed to be devoid of estrogen receptors (ERs) and have been widely used to study the functions of ER-alpha and ER-beta after transfection of their cDNAs. Numerous studies have demonstrated that transfected ER-alpha or ER-beta mediates estradiol-induced activation of multiple signaling pathways, including the MAPK/ERK pathways. We report here for the first time that both 17alpha-estradiol and 17beta-estradiol elicit activation of MAPK/ERK in native, nontransfected CHO-K1, COS-7, and Rat2 fibroblast cell lines. We further report that, contrary to the generally held belief, these cell lines are not unresponsive to estradiol in their native, nontransfected state, and that this estrogen responsiveness is associated with estrogen binding. Using multiple ER antibodies, we failed to find ER-alpha or ER-beta isoforms or even ER-X. In view of these findings, researchers, using such cells as models to investigate mechanisms of estrogen action, must always take into account the existence of endogenous estrogen binding proteins other than ER-alpha, ER-beta, or ER-X.