The

readings of chest expansion measurement showed 2.5 cm in the axillary level and 3 cm in the xiphoid level. Since the patient did not show stable clinical and biochemical factors (pH: 7.18, PaO2: 80, PaCO2: 50, HCO3: 27, and Base Excess: +1), a tilt table method of intervention was initiated. Tilt table procedure was carried out to preclude bed rest complications, and to promote ventilation along with routine chest physiotherapy. Tilt Table Protocol On 20th September 2009, the patient was held to lie on the tilt table with chest, pelvic and knee straps. Enough padding was provided over the chest when applying the chest strap. The chest strap was secured comfortably, so that the patient could breathe comfortably, Inhibitors,research,lifescience,medical and the vital signs were assured to prove hemodynamic

stability. Initially Inhibitors,research,lifescience,medical tilt table was propped up for 10 degrees, and blood pressure and pulse oximetry saturation were checked. When there was a drop in blood pressure (<100 mmHg) and saturation (<85% oxygen saturation), the tilt table was returned back to supine position. If the blood pressure and Inhibitors,research,lifescience,medical oxygen saturation were not satisfactory, the position preserved and the subject was asked to do breathing exercises. Further tilting to 45 degrees was performed slowly and progressively, if the patient condition was stable and satisfactory on clinical and biochemical factors. The total session lasted for 30 minutes (figure 1 and ​and2).2). Then SRT1720 order active breathing exercises, active assisted exercises of both upper and lower limb, Inhibitors,research,lifescience,medical and active exercises of both upper limbs and lower limbs were carried out along with the synchrony of ventilator. When the patient reached a progression of 60 to 90 degrees in the tilt table, ambulation was carried Inhibitors,research,lifescience,medical out on an ambulatory chair. Figure 1 The patient tilted on the tilt table and does functional activities training while on ventilator. Figure 2 Patient tilted to 60 degrees on the tilting table. The therapist performs active assisted exercises as the patient is on the ventilator support The tilt table protocol was carried out on a daily basis as an adjunct to other chest physiotherapy techniques including

active assisted and active exercises of both upper and lower limbs, and ambulation on an ambulatory chair was carried almost out on alternate days during the period 24th to 28th September 2009. After a week of tilting protocol, the patient showed progression in arterial blood gases (pH: 7.35, PaO2: 95, PaCO2: 40, HCO3: 22, and Base Excess: +1). He was able to breathe with CPAP continuously when he was awake. Then the patient was able to withstand without CPAP support for 6 hours. During the tilt table procedure on the fourth week, the patient managed to withstand tilt table without ventilator. The lung fields were clear in the chest x-ray. Chest expansion measurement also improved with 3 cm in axillary level and 3.5 cm in xiphoid level.

In the present study, personnel from the department of Clinical Physiology brought the isotope to the ED and injected it into the patient. If this is not practical, implementation of

MPI in routine care will likely require training of ED personnel, adoption of guidelines for handling isotopes, and perhaps even rebuilding rooms for radiation safety. MPI would probably not be suitable for centers where nuclear cardiology experts are not present or where the patient volume is small. With an annual attendance at our ED of some 65000 patients, we predict that Inhibitors,research,lifescience,medical there will be one or two patients per 24 h suitable for acute MPI. Due to the relatively high cost of the MPI itself, it seems important to ascertain that only patients who would otherwise be Romidepsin solubility dmso admitted to in-hospital Inhibitors,research,lifescience,medical care are referred to MPI. If not, as with any new diagnostic test, there is a risk of overuse which would decrease the potential cost savings. Another risk is that false positive MPI results induce unnecessary and expensive further testing, which will also reduce cost savings. When implementing MPI in routine care, it seems essential to inform the physicians about the very low PPV in these patients. Several other new diagnostic

methods have been suggested to be of value in the chest pain patient with suspected Inhibitors,research,lifescience,medical ACS [6]. Coronary angiography using multidetector CT scanning (MDCT) has shown promising results and in a meta-analysis by Vanhoenacker et al. the Inhibitors,research,lifescience,medical pooled sensitivity and specificity were 95% and 90% [20] in detecting non-ST-elevation ACS. MDCT has the advantage over MPI to be a very rapid investigation and to be available in more centers and more often outside office hours. MDCT also has the potential to detect other causes of chest pain than acute cardiac disease. A disadvantage with MDCT is that it exposes the patient to a larger radiation dose (5–20 mSv) than rest MPI. Extending MPI availability outside office hours

would most likely increase the cost per MPI investigation. The exact cost increase will of course be different at every center, but a larger patient volume than ours Inhibitors,research,lifescience,medical would probably these be needed to make an on-call physician and standby isotope economically feasible. In our hospital, about one patient a day during office hours can be acutely imaged within the existing capacity of the MPI-cameras. Limitations Our study only included a small fraction of the potentially eligible subjects during the study period, which in theory could lead to a selection bias. There were however no systematic criteria for patient selection other than the inclusion criteria described in Methods, and the included patients were therefore considered to be a random sample of all eligible patients. The patients included in this study were on average eight years younger than our chest pain patients in general [21]. This probably reflects our exclusion criteria (e.g.

Footnotes This study was supported by a grant from the Ontario Ministry of Health and Long-Term Care (MOHLTC) Drug Innovation Fund and the Institute for Clinical Evaluative Sciences (ICES), a non-profit research institute sponsored by the Ontario MOHLTC. Dr Paul Kurdyak is supported by a Canadian Institutes of Health Research (CIHR) New Investigator Award. We thank Brogan Inc., Ottawa for use of their Drug Product Inhibitors,research,lifescience,medical and Therapeutic Class Database. Muhammad M.

Mamdani has carried out consultancy work for Hoffman LA Roche Advisory Boards, GSK, Pfizer, Novartis, EI Lilly, Novo Nordisk, Astra Zeneca, and Bristol Myers Squid. The other authors have no conflict of interests to declare.
Objective: Brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF) and leptin have been hypothesized to be involved in the neurobiology of depression. The aim of this study was to investigate BDNF, VEGF and leptin levels in patients Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical with severe EPZ5676 chemical structure melancholic depression. Methods: A total of 40 drug-free patients with major depressive

disorder (MDD) with melancholic features and 40 healthy controls were included in the study. Demographic information, psychiatric evaluation and physical examination were documented for both groups. Serum BDNF, VEGF levels were determined by enzyme-linked immunosorbent assay and leptin with radioimmunoassay methods. The Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale were applied to the

patients. Results: There were no significant differences in serum BDNF, VEGF Inhibitors,research,lifescience,medical and leptin levels between the patient and control groups. There was a negative correlation between BDNF Inhibitors,research,lifescience,medical levels and the number of depressive episodes. It was noted that VEGF levels decreased with increasing severity of depression. Conclusions: These findings suggest that BDNF levels might be associated with the recurrence of depression and VEGF levels might be a determinant of the severity of depression. Keywords: brain-derived neurotrophic Unoprostone factor, depression, leptin, vascular endothelial growth factor Introduction Major depressive disorder (MDD) is a devastating disease that afflicts approximately 8% of men and 15% of women [Kessler et al. 1994]. Approximately 25–30% of depressed patients are classified as ‘melancholic type’ [Rush and Weissenburger, 1994]. Clinical research has demonstrated that melancholic type-depressed patients are less likely to respond to placebo therapy, supporting the hypothesis of a biological foundation and the need for suitable pharmacotherapy [Peselow et al. 1992].

This could be related to a reporting bias, as neurologists may not recognize or describe mild disorganization. Indeed, we were able to observe one patient scoring 4 on the Positive And Negative Syndrome Scale (PANSS) disorganization subscore. The symptom lasted during a relapse of her MS, and was accompanied by a clear reduction in executive attention without confusion or mood disorder. However, more observations arc required in order to conclude. It is even more difficult

Inhibitors,research,lifescience,medical to conclude concerning negative symptoms which are also an important feature of schizophrenia, because they can be misidcntificd with depression or cognitive decline. What kind of white matter lesion is most likely to evoke psychosis? Inhibitors,research,lifescience,medical WM lesions can have two different physiological effects: From reduction to absence of conduction between two areas. This concept is closer to the notion of deconncction. A variation in conduction time between the different axons linking the two areas. This is what we termed “disconnection.” Synapses will not be active in the same time window, resulting in an improper

summation in the postsynaptic neurons. Not only will the message be weakened, but it will also be noisier. MS and MLD essentially result in lengthening and scattering of conduction delays.100 Demyelinating diseases can also induce voltage-gated channel anomalies Inhibitors,research,lifescience,medical that result in conduction bloc (analogous to deconnection).101 However, MS and MLD seem to trigger more psychotic episodes than diffuse axonal injury after a head trauma Inhibitors,research,lifescience,medical that basically results in a deconnection.102- Accordingly, there is modest evidence that a dis-synchrony between axons better accounts for psychosis. Misconnectivity Misconnectivity is perhaps even more difficult to model, because it can involve different neurons. However, multiple neurological diseases come with putative misconnectivity, especially when accompanied by cortical

dysplasia or heterotopia. Some of them have been described Inhibitors,research,lifescience,medical as presenting with psychosis: Schizencephaly-polymicrogyria.103 Ito’s disease.101 Facomatosis as tuberous sclerosis, also termed Bourneville’s disease.105 In another facomatosis, neurofibromatosis type 1, or Recklinghausen’s disease, about 3% to 6% of patients develop psychosis.106,107 However the amount of psychosis in misconncction diseases is mild. It could also not be the causal factor, as most of these disorders are accompanied Edoxaban by epilepsy. But from an other perspective, the psychosis of epilepsy has not been found to be related to dysplasia.108 Another confounding factor could be the presence of WM lesions in most misconnection diseases. As an example, both tuberous sclerosis and neurofibromatosis also come with WM abnormalities that could account for the expression of psychosis.109-110 Interestingly, psychosis related to cortical dysplasia can appear earlier than adolescence.106 According to our previous line of Selleckchem LY3009104 reasoning, this could mean that dopamine is not an important cofactor.

biomedcentral.com/1471-227X/9/3/prepub Supplementary Material Additional file 1: The Consort Flowchart. The Graph provided shows the Consort flowchart of the

study. Click here for file(36K, doc) Acknowledgements Partly supported by a grant of the Swiss National Foundation. The funding source had no involvement in the study design; collection, analysis, and interpretation Inhibitors,research,lifescience,medical of the data; in the SIRT2 protein writing of the manuscript; and in the decision to submit the manuscript for publication.
The use of anion gap assessment to interpret and diagnose the etiology of metabolic acidosis was originally described by Emmet and Narins in 1977.[1] Lactic acid, a “gap” acid, is one cause of elevated Inhibitors,research,lifescience,medical anion gap metabolic acidosis,

and an elevated serum lactate level has emerged as an important tool to screen for patients in shock. Elevated serum lactate can be caused by inadequate perfusion, but may also be a product of inflammation, cytopathic hypoxia, and increased rates of glycolysis. [2-4] In critically ill patients, an elevated lactate level is indicative of increased severity of illness and subsequent serum lactate clearance predicts an improved outcome.[5,6] Rivers et al, utilized hypotension and elevated serum lactate levels to identify patients in shock and demonstrated that emergency department patients with presumed sepsis Inhibitors,research,lifescience,medical and a serum lactate level of ≥ 4.0 mmol/L and/or frank hypotension are at a significant risk of death (38–59% mortality).[7] Despite this study and multiple other investigations that document the value of measuring serum lactate concentrations, the measurement of serum lactate is still not routine.

In fact, in some institutions, serum lactate remains a “send out” Inhibitors,research,lifescience,medical test (unpublished data, Table ​Table1).1). We believe that one reason the measurement of serum lactate is not part of a standard admission battery of laboratory tests is that clinicians assume other commonly measured and calculated Inhibitors,research,lifescience,medical lab values, such as anion gap (AG) and base deficit (BD), accurately identify the presence or absence of hyperlactatemia. Despite previous studies showing that neither base deficit nor anion gap are effective at discriminating between the presence or absence of hyperlactatemia, [8-12] there persists the commonly unless held belief that a normal anion gap or the absence of base deficit rules out the presence of hyperlactatemia. Table 1 Availability of serum lactate in Washington DC metro area hospitals One possible reason for this discrepancy is that hypoalbuminemia, a common finding in critically ill patients, can cause a decrease in the “normal” measured anion gap and thereby mask the presence of an elevated anion gap.[13] Therefore, some investigators have suggested that anion gap corrected for albumin (ACAG) is a more appropriate screening tool for the diagnosis of metabolic acidosis in the ICU.

19 The development of a product and its refinement over selleck chemicals llc several years started from a very few devoted clinicians who believed that a scaffold that dissolves over several months is

better than a metal stent that becomes part of the arterial wall, persisting throughout the patient’s life. A similar approach, only with a metal, has been done with an absorbable magnesium stent.20 Only time will tell whether this technology will have additional benefit for patients. The valvular Inhibitors,research,lifescience,medical revolution that we are witnessing today is another example of very intense developments involving all corners of the triangle. With the ability to implant an aortic stent via catheterization, transarterial aortic valve replacement (TAVR) was conceived by physicians and is currently applied to high-risk patients with aortic stenosis.21 This ability was made possible by refining and combining metal stent and biological valve technologies. It is an amazing Inhibitors,research,lifescience,medical tool, and currently

aortic stent interventions are at a rapid expansion Inhibitors,research,lifescience,medical phase with proven evidence by large controlled randomized studies. The success in aortic stent devices stimulated and triggered multiple attempts to expand the horizon to new frontiers in the mitral space.22 Again, as in the early stent era, we see a plethora of innovative ideas, using the model of new startup companies that always involved a combination of passionate physician-scientists and a strong and capable engineering core. STEM CELLS AND BEYOND The area of human embryonic stem cell technology

was introduced by Thomson et al.23 in 1998, through a collaborative effort between the University of Wisconsin and academic work performed at Rambam Health Care Campus and Inhibitors,research,lifescience,medical the Technion Inhibitors,research,lifescience,medical in the Laboratory of Joseph Itskovitz. The first human stem lines in the world are therefore the outcome of an outstanding collaboration between academia (Technion and the University of Wisconsin) and a clinical hospital (Rambam Health Care Campus). This work was followed by an explosive growth in the field worldwide, stirring a plethora of ethical concerns among countries, societies, politicians, and religious bodies. Even established government research bodies such as the NIH had to apply ethical rules imposed on them by political leaders. Despite these limitations, this field was vibrant with activity. Differentiation into cardiac 4-Aminobutyrate aminotransferase cells was shown by Kehat et al. from the Technion and Rambam Hospital,24 and others have also shown differentiation into nerve and other cell types. Fueled by objections and debate, this field has generated much enthusiasm and hope for curing cardiovascular, neurological, metabolic, and other diseases. It has also reached a phase of early pilot clinical studies in several applications; however, to date, it has not shown a clear and proven benefit.

Therefore, STA-4783 post-operative nausea and vomiting are more common and these patients in these patients.10 In the present study, the incidence rates

of PONV in the placebo, dexamethasone and ondansetron groups were 100%, 54.8% and 49.3%, respectively. The incidence rate and intensity of PONV in the dexamethasone and ondansetron groups were significantly lower than that in the control group. Inhibitors,research,lifescience,medical In the final stages of the study, incidence rate and intensity of PONV in the dexamethasone group was less than that in the ondansetron group. Previous studies have shown that compared to distilled water, intravenous dexamethasone significantly reduced the rate and intensity of the PONV.11-13 Limited studies have compared the effects of dexamethasone and ondansetron on PONV, Inhibitors,research,lifescience,medical and their findings are contradictory. Erhan et al. conducted a comparative study on ondansetron (4 mg IV), granisteron (3 mg IV) and dexamethasone (8 mg IV) effects given before induction of anesthesia to prevent postoperative PONV in laparoscopic cholecystectomy. They showed that compared to placebo all the three drugs in similar manner significantly reduced the incidence rate of PONV.14 Lopez-Olaondo et al. reported Inhibitors,research,lifescience,medical that dexamethasone was as effective as ondansetron in reducing nausea and vomiting induced by chemotherapy.15 Gupta also concluded that intravenous dexamethasone and ondansetron had a similar effect on PONV prevention.16

Moreover, Munoz et al. showed that the effects Inhibitors,research,lifescience,medical of dexamethasone and ondansetron in preventing PONV were similar.17 However, in another study,18 it was shown that ondansetron was better than dexamethasone. Another study showed that dexamethasone was a little

more effective than ondansetron in preventing post-tonsillectomy PONV.19 Also, a study of 60 patients undergoing laparoscopic cholecystectomy showed that the incidence rate of Inhibitors,research,lifescience,medical PONV in the dexamethasone group was significantly lower (20% versus 43.3%).20 The difference in the findings of the above studies might be related to wide range of differences in sample sizes, patients qualities, type of surgical operations and anesthetic techniques, the way that PONV was defined and studied, and most important of all the dosage (-)-p-Bromotetramisole Oxalate of the antiemetic drugs and the timing of their administration.17,21 The present study showed that dexamethasone was more effective than ondansetron in preventing PONV; therefore, it may be more suitable to be administered in such a situation. In the studies in which no difference was reported between dexamethasone and ondansetron, the use of dexamethasone was preferred. This might be attributed to the lower cost of dexamethasone than that of ondansetron.14 The present study showed that neither dexamethasone nor ondansetron was associated with no significant side effects. The safety of these drugs has already been confirmed.

Surgical attention must be given to the creation of fresh frozen specimen banks, as sensitivity of mutation detection may be higher in fresh frozen rather than paraffin embedded specimens.

The role of other mutations, such as K-RAS, predictive of response to EGFR inhibition with monoclonal antibodies in colon cancer, needs further investigation in these diseases. Future targeted therapy should take into account treatment regimens- as monotherapy or in combination with current chemotherapy. Acknowledgements Disclosure: The authors declare no conflict of interest.
Once peritoneal metastases occur from gastrointestinal cancers or mesothelioma, morbidity and mortality are almost always secondary Inhibitors,research,lifescience,medical to disease progression within the abdominal cavity. Inhibitors,research,lifescience,medical Patients experience progressive abdominal distention due to tumor growth and malignant ascites, pain, early satiety, and ultimately experience profound cachexia and inanition (1). The condition is characterized grossly by diffuse tumor nodules on the peritoneal surfaces; the omentum is a favored site for development of extensive bulky metastases which is typically referred to as “omental caking” on preoperative imaging studies. Tissue is usually obtained by laparoscopic or percutaneous biopsy and the histologic features of the tumor combined with other clinical, laboratory, or imaging click here findings

can successfully identify Inhibitors,research,lifescience,medical the tumor site of origin. According to the multicenter EVOCAPE I study (2), the median survival in patients with peritoneal metastases was 5.2 months for those with advanced colorectal cancer (n=118) Inhibitors,research,lifescience,medical and 3.1 months for those with advanced gastric

cancer (n=125). Despite significant advances in the development of more efficacious Inhibitors,research,lifescience,medical systemic chemotherapy for many GI cancers, most notably colorectal cancer; systemic treatment is associated with potentially severe toxicity in many patients and median survival is still less than two years (Table 1). Mesothelioma is very rare with 200-400 new cases diagnosed annually in US, its incidence Amisulpride is increasing and expected to reach a peak in 2020 in Europe (3). Table 1 Survival in patients with peritoneal dissemination secondary to various cancers based on variability in tumor biology Systemic chemotherapy for advanced GI cancers and mesothelioma It is important to briefly review the efficacy and toxicity of various systemic chemotherapy regimens commonly used for patients with advanced GI cancers or mesothelioma to provide context and better understand the potential role of cytoreduction surgery (CRS) and HIPEC. Over the past 6 years there have been several new chemotherapeutic and biological agents that have been approved by the FDA for treatment of patients with advanced colorectal cancer. One common regimen is 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) combined with bevacizumab. Saltz et al.

Footnotes Conflict of interest: No potential conflict of interest relevant to this article was reported.
Celiac disease (CD) is an autoimmune disorder occurring in genetically susceptible subjects. CD is the only autoimmune

disease where the target of the immune reaction, namely gluten, has been identified. The incidence of CD is around 1%, and it is much more common in first-degree relatives of CD patients, 10%–18%. However, the pattern of the genetic inheritance is still obscure. The proteins blamed for causing CD are the peptic-tryptic digest of gluten, namely gliadin, Inhibitors,research,lifescience,medical the wheat prolamines, and the related prolamines from rye and barley. Currently, the oat prolamines are considered safe in most but not all CD patients.1,2 ENVIRONMENTAL FACTORS Environmental factors are undoubtedly affecting the disease’s clinical presentation, time at presentation, and may affect the characteristics Inhibitors,research,lifescience,medical of the disease. There are claims that controlling some of the environmental factors might affect the development of CD. Several studies towards the end of the previous century demonstrated

that breastfeeding reduced the incidence Inhibitors,research,lifescience,medical of developing CD. Was it a real prevention or just postponing its appearance, as was demonstrated later by Maki’s group from Finland?3 This group demonstrated that breastfeeding does indeed postpone the development of the disease in its classical presentation, Inhibitors,research,lifescience,medical to appear later in life with either symptoms derived from malabsorption, such as anemia or bone disorder, or as an extra-intestinal manifestation

of CD, such as insulin-dependent GDC 0449 diabetes mellitus (IDDM) and rheumatoid arthritis. Recently, Norris et al.4 demonstrated that introducing small amounts of gluten Inhibitors,research,lifescience,medical to infants from 4–6 months old while still breastfeeding decreased the incidence of CD in a risk group for developing CD (HLADQ2 and/or DQ8-positive subjects).5 Infectious agents might have a role, at least on the timing of the presentation of CD or even on its incidence. A sequence homology between the toxic peptide of gliadin and enteric type Adenovirus was demonstrated by Kagnoff et al.6 Recently, Stene et al.7 demonstrated that exposure to two or more serotypes Oxymatrine of Rotavirus is statistically significantly more common in CD. Adherence of bacterial agents to the small bowel intestinal mucosa was found in CD patients, but not in control subjects.8 Nieuwenhuizen et al.9 demonstrated that the virulent factor of Candida albicans—hyphal wall protein 1—shares similar sequence homology of amino acids with gliadin. PATHOGENESIS In a celiac-susceptible subject with the specific HLADQ2 and/or DQ8, under stressful situations (such as infection, surgery, etc.), the gliadin enters the lamina propria where it is deamidated by the enzyme tissue transglutaminase (tTG) and then becomes attached to it.

” “Hoping against hope” is the tension between

hoping for a cure for their family member and the recognition that this is no longer a possibility. At the same time they had other types of hope. Hope for these participants was also a choice and a mindset. Many women wrote about how they tried their best, Epacadostat nmr despite extremely discouraging circumstances, to look for hope each and every day in the simple things, and in focusing on the present. They chose to look for the positive aspects of each day and also resorted to good memories of the lives they had lived with the care Inhibitors,research,lifescience,medical receiver. Choosing to be hopeful was not easy, and part of this mindset also involved acceptance of their circumstance, and striving to find a new ‘normal’ amidst so much uncertainty. The new normal and acceptance is described here by two participants: “Now we have adapted to the new normal. We are still optimistic… I guess we both know the odds are not in our favour but it is hard to do anything else but Inhibitors,research,lifescience,medical push into it and hope for the best.” “I know that we have changed our expectations of what is possible for our family and that’s ok. I think that my family has all adjusted to what our new “normal” is and we are trying

to embrace Inhibitors,research,lifescience,medical our opportunities right now.” Participants described several influences on their hope: temporal circumstances, social support, spirituality and faith. Circumstances The specific, temporal circumstances of each day could foster or take away from the participants’ hope. Caregivers’ levels of hope and their general mood were heavily dependent on the mood Inhibitors,research,lifescience,medical of the care recipient and the care receiver’s state of health. Good

days were more hopeful days. The weather and environment played a role in the caregivers’ perceptions of their hope, as one participant shared, “Hope, Inhibitors,research,lifescience,medical well it was hard to find any today except that the flowers are blooming beautifully, and that is something.” Factors that detracted from the participants’ hope were dreary weather, stressful travel and medical appointments, family conflict, and the declining health and well-being of the care receiver. One participant described her stress with driving and how she felt alone: “I feel alone even Farnesyltransferase when people are here! Nobody really understands! [Care receiver] is sick. I need to lift him into the truck… I am scared of getting him into the truck tomorrow to go to [location of appointment].” Social support Social support was found to be a key theme that fosters hope, whether this was support from family members, friends or health professionals such as doctors and nurses. Many caregivers mentioned how celebrating an occasion with family members, seeing their grandchildren, having extra support from their sons and daughters or their siblings, brought hope to their day and to their lives, for example, “Our friends and our health team give me hope for tomorrow… my support if & when [care receiver] needs them or we need them.