We systematically reviewed the evidence from animal studies assessing the effects of pentoxifylline on neonatal hypoxic-ischemic encephalopathy (HIE). The PubMed, EMBASE, EMCARE, MEDLINE, Cochrane Library, and Google Scholar databases were searched for randomized and quasi randomized controlled trials (RCTs) in December 2023 to determine the effects of pentoxifylline in animal models of HIE. The quality of the included studies was assessed via the SYRCLE risk of bias (ROB) tool. The certainty of evidence was assessed via the GRADE methodology. All seven included studies (n = 248) involved a rat HIE model in which pentoxifylline (25–150 mg/kg) was administered intraperitoneally. The majority had unclear ROB. All the studies reported a protective effect of pentoxifylline on HIEinduced organ injury. Mortality was comparable at pentoxifylline doses between 25 and 75 mg/kg but higher at 150 mg/kg than in the control group. Three studies reported macroscopic changes in HIE-affected organs. There was a significant reduction in cerebral infarction (40 and 75 mg/kg), hippocampal atrophy, and visible gut injury (60 mg/kg). A significantly lower number of Caspase 3 immunoreactive cells and necrotic cells were observed at the 60 mg/kg dose, whereas the 100 mg/kg dose had a deleterious effect. Three other studies reported significantly reduced levels of proinflammatory markers including IL-6 and TNF-alpha. Current evidence (with low uncertainty) from a rat model suggests that pentoxifylline has the potential to improve mortality and attenuate organ injury following HIE. Adequately powered, well-designed human RCTs are needed to confirm our findings.

We systematically reviewed the evidence from animal studies assessing the effects of pentoxifylline on neonatal hypoxic-ischemic encephalopathy (HIE). The PubMed, EMBASE, EMCARE, MEDLINE, Cochrane Library, and Google Scholar databases were searched for randomized and quasi randomized controlled trials (RCTs) in December 2023 to determine the effects of pentoxifylline in animal models of HIE. The quality of the included studies was assessed via the SYRCLE risk of bias (ROB) tool. The certainty of evidence was assessed via the GRADE methodology. All seven included studies (n = 248) involved a rat HIE model in which pentoxifylline (25–150 mg/kg) was administered intraperitoneally. The majority had unclear ROB. All the studies reported a protective effect of pentoxifylline on HIEinduced organ injury. Mortality was comparable at pentoxifylline doses between 25 and 75 mg/kg but higher at 150 mg/kg than in the control group. Three studies reported macroscopic changes in HIE-affected organs. There was a significant reduction in cerebral infarction (40 and 75 mg/kg), hippocampal atrophy, and visible gut injury (60 mg/kg). A significantly lower number of Caspase 3 immunoreactive cells and necrotic cells were observed at the 60 mg/kg dose, whereas the 100 mg/kg dose had a deleterious effect. Three other studies reported significantly reduced levels of proinflammatory markers including IL-6 and TNF-alpha. Current evidence (with low uncertainty) from a rat model suggests that pentoxifylline has the potential to improve mortality and attenuate organ injury following HIE. Adequately powered, well-designed human RCTs are needed to confirm our findings.

We systematically reviewed the evidence from animal studies assessing the effects of pentoxifylline on neonatal hypoxic-ischemic encephalopathy (HIE). The PubMed, EMBASE, EMCARE, MEDLINE, Cochrane Library, and Google Scholar databases were searched for randomized and quasi randomized controlled trials (RCTs) in December 2023 to determine the effects of pentoxifylline in animal models of HIE. The quality of the included studies was assessed via the SYRCLE risk of bias (ROB) tool. The certainty of evidence was assessed via the GRADE methodology. All seven included studies (n = 248) involved a rat HIE model in which pentoxifylline (25–150 mg/kg) was administered intraperitoneally. The majority had unclear ROB. All the studies reported a protective effect of pentoxifylline on HIEinduced organ injury. Mortality was comparable at pentoxifylline doses between 25 and 75 mg/kg but higher at 150 mg/kg than in the control group. Three studies reported macroscopic changes in HIE-affected organs. There was a significant reduction in cerebral infarction (40 and 75 mg/kg), hippocampal atrophy, and visible gut injury (60 mg/kg). A significantly lower number of Caspase 3 immunoreactive cells and necrotic cells were observed at the 60 mg/kg dose, whereas the 100 mg/kg dose had a deleterious effect. Three other studies reported significantly reduced levels of proinflammatory markers including IL-6 and TNF-alpha. Current evidence (with low uncertainty) from a rat model suggests that pentoxifylline has the potential to improve mortality and attenuate organ injury following HIE. Adequately powered, well-designed human RCTs are needed to confirm our findings.

We systematically reviewed the evidence from animal studies assessing the effects of pentoxifylline on neonatal hypoxic-ischemic encephalopathy (HIE). The PubMed, EMBASE, EMCARE, MEDLINE, Cochrane Library, and Google Scholar databases were searched for randomized and quasi randomized controlled trials (RCTs) in December 2023 to determine the effects of pentoxifylline in animal models of HIE. The quality of the included studies was assessed via the SYRCLE risk of bias (ROB) tool. The certainty of evidence was assessed via the GRADE methodology. All seven included studies (n = 248) involved a rat HIE model in which pentoxifylline (25–150 mg/kg) was administered intraperitoneally. The majority had unclear ROB. All the studies reported a protective effect of pentoxifylline on HIEinduced organ injury. Mortality was comparable at pentoxifylline doses between 25 and 75 mg/kg but higher at 150 mg/kg than in the control group. Three studies reported macroscopic changes in HIE-affected organs. There was a significant reduction in cerebral infarction (40 and 75 mg/kg), hippocampal atrophy, and visible gut injury (60 mg/kg). A significantly lower number of Caspase 3 immunoreactive cells and necrotic cells were observed at the 60 mg/kg dose, whereas the 100 mg/kg dose had a deleterious effect. Three other studies reported significantly reduced levels of proinflammatory markers including IL-6 and TNF-alpha. Current evidence (with low uncertainty) from a rat model suggests that pentoxifylline has the potential to improve mortality and attenuate organ injury following HIE. Adequately powered, well-designed human RCTs are needed to confirm our findings.

We systematically reviewed the evidence from animal studies assessing the effects of pentoxifylline on neonatal hypoxic-ischemic encephalopathy (HIE). The PubMed, EMBASE, EMCARE, MEDLINE, Cochrane Library, and Google Scholar databases were searched for randomized and quasi randomized controlled trials (RCTs) in December 2023 to determine the effects of pentoxifylline in animal models of HIE. The quality of the included studies was assessed via the SYRCLE risk of bias (ROB) tool. The certainty of evidence was assessed via the GRADE methodology. All seven included studies (n = 248) involved a rat HIE model in which pentoxifylline (25–150 mg/kg) was administered intraperitoneally. The majority had unclear ROB. All the studies reported a protective effect of pentoxifylline on HIEinduced organ injury. Mortality was comparable at pentoxifylline doses between 25 and 75 mg/kg but higher at 150 mg/kg than in the control group. Three studies reported macroscopic changes in HIE-affected organs. There was a significant reduction in cerebral infarction (40 and 75 mg/kg), hippocampal atrophy, and visible gut injury (60 mg/kg). A significantly lower number of Caspase 3 immunoreactive cells and necrotic cells were observed at the 60 mg/kg dose, whereas the 100 mg/kg dose had a deleterious effect. Three other studies reported significantly reduced levels of proinflammatory markers including IL-6 and TNF-alpha. Current evidence (with low uncertainty) from a rat model suggests that pentoxifylline has the potential to improve mortality and attenuate organ injury following HIE. Adequately powered, well-designed human RCTs are needed to confirm our findings.

The development of refractory ascites in approximately 10% of patients with decompensated cirrhosis heralds the progression to a more advanced stage of cirrhosis. Its pathogenesis is related to significant hemodynamic changes, initiated by portal hypertension, but ultimately leading to renal hypoperfusion and avid sodium retention. Inflammation can also contribute to the pathogenesis of refractory ascites by causing portal microthrombi, perpetuating the portal hypertension. Many complications accompany the development of refractory ascites, but renal dysfunction is most common. Management starts with continuation of sodium restriction, which needs frequent reviews for adherence; and regular large volume paracentesis of 5 L or more with albumin infusions to prevent the development of paracentesisinduced circulatory dysfunction. Albumin infusions independent of paracentesis may have a role in the management of these patients. The insertion of a covered, smaller diameter, transjugular intrahepatic porto-systemic stent shunt (TIPS) in the appropriate patients with reasonable liver reserve can bring about improvement in quality of life and improved survival after ascites clearance. Devices such as an automated low-flow ascites pump may be available in the future for ascites treatment. Patients with refractory ascites should be referred for liver transplant, as their prognosis is poor. In patients with refractory ascites and concomitant chronic kidney disease of more than stage 3b, assessment should be referred for dual liver-kidney transplants. In patients with very advanced cirrhosis not suitable for any definitive treatment for ascites control, palliative care should be involved to improve the quality of life of these patients.

OBJECTIVES: This study examined breast cancer screening (BCS) practices and its associated factors among menopausal and postmenopausal women. METHODS: A cross-sectional design was conducted using convenience sampling at a community center. The modified Chinese BCS Belief questionnaire was used to understand BCS practice. RESULTS: A total of 144 eligible women presented better knowledge and perceptions about breast cancer (mean, 11.46; standard deviation [SD], 3.65) and barriers to achieving mammographic screening (mean, 14.75; SD, 3.70). Participants aged ≥ 50 years had a negative association with the attitudes towards general health check-ups (B = −1.304, standard error [SE] = 0.65, P = 0.046). In this context, having regular physical exercise had a positive association with attitudes towards general health check ups (B = 1.458, SE = 0.06, P = 0.017), and knowledge and perceptions about breast cancer (B = 1.068, SE = 0.62, P = 0.086). Being employed had a positive associated with barriers to achieving mammographic screening (B = 1.823, SE = 0.51, P < 0.001). CONCLUSIONS: The women had better knowledge and perception about breast cancer and fewer barriers to mammographic screening. However, attitudes towards general health check-ups were relatively poor. It is noteworthy that women who aged ≥ 50 years and had insufficient physical exercise had poor attitudes. Those who were employed had fewer barriers, and those who had regular physical exercise had better knowledge on the benefits of the BCS practice. Importantly, women who aged ≥ 50 years and lack physical exercise need education about breast cancer to increase their awareness of breast wellness.
Asian Continental Ancestry Group ; Breast Neoplasms ; Breast ; Education ; Exercise ; Female ; Humans ; Mass Screening ; Menopause ; Postmenopause ; Women's Health

The one co-author (Florence MF Wong) was missing in the original version of this article.

The traditional diagnostic criteria of renal dysfunction in cirrhosis are a 50% increase in serum creatinine (SCr) with a final value above 1.5 mg/dL. This means that patients with milder degrees of renal dysfunction are not being diagnosed, and therefore not offered timely treatment. The International Ascites Club in 2015 adapted the term acute kidney injury (AKI) to represent acute renal dysfunction in cirrhosis, and defined it by an increase in SCr of 0.3 mg/dL (26.4 µmoL/L) in <48 hours, or a 50% increase in SCr from a baseline within ≤3 months. The severity of AKI is described by stages, with stage 1 represented by these minimal changes, while stages 2 and 3 AKI by 2-fold and 3-fold increases in SCr respectively. Hepatorenal syndrome (HRS), renamed AKI-HRS, is defined by stage 2 or 3 AKI that fulfils all other diagnostic criteria of HRS. Various studies in the past few years have indicated that these new diagnostic criteria are valid in the prediction of prognosis for patients with cirrhosis and AKI. The future in AKI diagnosis may include further refinements such as inclusion of biomarkers that can identify susceptibility for AKI, differentiating the various prototypes of AKI, or track its progression.
Acute Kidney Injury/complications/*diagnosis/drug therapy/pathology ; Biomarkers/blood ; Creatinine/blood ; Humans ; Liver Cirrhosis/*complications ; Prognosis ; Serum Albumin/therapeutic use ; Severity of Illness Index