Miracle-dz/UniFAR-FTUs huggingface dataset:
Consequences of malnutrition in early life and strategies to improve maternal and child diets through targeted fortified products.

This supplement brings together papers focusing onthe critical 1000 days of human development frompregnancy until 2 years of age. It is the third in anannual series ﬁrst published as a Special SupplementoftheFoodandNutritionBulletininJune2009.Dietsof poor nutritional quality during pregnancy, infancyandearlychildhoodleadtonutrientintakes,whichdonot meet requirements.This, combined with frequentinfections during early childhood,results in deﬁcits ingrowth (stunting),limited psychosocial development,increased risk of mortality, and reduced learningcapacity and productivity later in life among thosethat survive. Programmes need to prevent these deﬁ-cits by improving maternal and child nutrient intakein addition to preventing and treating infections.Over the past 3 years, the community of nutritionscientists and researchers, activists and developmentpractitioners committed to an integrated approach tonutrition programming has grown. This communityadvocates for a greater focus on maternal, infant andyoung child nutrition (MIYCN), the application of alifecycle approach to programming and the breakingdown of the barriers between expertise and sectorsthat limit the scale-up of cost-effective programmesthat meet the needs of vulnerable populations on asustainedbasis. ThisMIYCNsupplementcontinuestoreﬂect and contribute to this movement by providingthe results of leading-edge research to inform techni-cal consensus, programme design, policy and furtherresearch. It discusses the consequences of malnutri-tion in early life and focuses on programme-relatedresearch to improve nutrient intake through breast-feeding, promoting consumption of special formu-lated fortiﬁed foods that ﬁll nutrient gaps or enhancethe diets of women and children. It also presentsresearch assessing feeding practices and preferencesof caregivers in relation to child feeding and formu-lated products. An operations research project inChina is described that illustrates how these activitieswerebroughttogetherinanintegratedprogrammetoimprove nutrient intake in young children.Dewey and Begum (2011) set the stage by summa-rizing the prevalence, causes and consequences ofstunting.One-third of children under 5 years of age indeveloping countries are stunted,with many childrenin several regions already stunted at birth. Stuntingrates increase during the ﬁrst 24 months of life withlittle change thereafter until adolescence, whendelayed maturation and an extended growth periodresult in some compensatory growth (Bosch
Angiotensin‐converting‐enzyme 2 inhibits liver fibrosis in mice

The renin‐angiotensin system (RAS) plays a major role in liver fibrosis. Recently, a homolog of angiotensin‐converting‐enzyme 1 (ACE1), termed ACE2, has been identified that appears to be a negative regulator of the RAS by degrading Ang II to Ang1‐7. The aim of this study was to characterize the long‐term effects of gene deletion of ACE2 in the liver, to define the role of ACE2 in acute and chronic liver disease, and to characterize the role of Ang1‐7 in hepatic stellate cell (HSC) activation. Ace2 knockout (KO) mice and wild‐type (wt) littermates underwent different models of acute and chronic liver injury. Liver pathology was analyzed by histology, immunohistochemistry, alpha smooth muscle actin (α‐SMA) immunoblotting, and quantitative polymerase chain reaction (qPCR). Murine HSCs were isolated by collagenase‐pronase‐perfusion, and density gradient centrifugation. One‐year‐old ace2 KO mice spontaneously developed an inflammatory cell infiltration and mild hepatic fibrosis that was prevented by treatment with irbesartan. Ace2 KO mice showed increased liver fibrosis following bile duct ligation for 21 days or chronic carbon tetrachloride (CCl4) treatment. In contrast, ace2 KO mice subjected to acute liver injury models did not differ from wt littermates. Treatment with recombinant ACE2 attenuated experimental fibrosis in the course of cholestatic and toxic liver injury. HSCs express the Ang1‐7 receptor Mas and Ang1‐7 inhibited Ang II‐induced phosphorylation of extracellular signal‐regulated kinase (ERK)‐1/2 in cultured HSCs. Conclusion: ACE2 is a key negative regulator of the RAS and functions to limit fibrosis through the degradation of Ang II and the formation of Ang1‐7. Whereas loss of ACE2 activity worsens liver fibrosis in chronic liver injury models, administration of recombinant ACE2 shows therapeutic potential. (HEPATOLOGY 2009.)
Nonalcoholic steatohepatitis in children: A multicenter clinicopathological study

Nonalcoholic fatty liver disease (NAFLD) may have distinct histological features in children and adults, but to date limited data are available on the spectrum and significance of histological lesions in pediatric patients. We conducted a multicenter study of children with well‐characterized, biopsy‐proven NAFLD to (1) assess the presence and significance of a constellation of histological lesions and (2) identify clinical and laboratory predictors of disease severity. One hundred thirty children with NAFLD seen from 1995 to 2007 in five centers in the United States and Canada were studied. Clinical and laboratory data were collected. Slides stained with hematoxylin‐eosin and trichrome were evaluated by two liver pathologists. The NAFLD activity score (NAS) and the pattern of liver injury (type 1 or adult versus type 2 or pediatric nonalcoholic steatohepatitis [NASH]) were recorded. Fibrosis was staged using a published 7‐point scale. The median age was 12 years (range, 4‐18 years); 63% were boys, and 52% were Caucasian. Fibrosis was present in 87% of patients; of these, stage 3 (bridging fibrosis) was present in 20%. No patient had cirrhosis. The median NAS was 4. Overlapping features of both type 1 (adult pattern) and type 2 (pediatric pattern) NASH were found in 82% of patients. Compared with patients with no or mild fibrosis, those with significant fibrosis were more likely to have higher lobular and portal inflammation scores (P < 0.01), perisinusoidal fibrosis (P < 0.001), and NAS ≥5 (P < 0.005). Serum aspartate aminotransferase levels were the only clinical or laboratory data that independently predicted severity of fibrosis (P = 0.003). Conclusion: Our results highlight the limitations of published proposals to classify pediatric NAFLD, and identified histological lesions associated with progressive disease. (HEPATOLOGY 2009.)
Binge Drinking Among Arab/Chaldeans: An Exploratory Study

Focus groups were conducted with young Arab/Chaldeans (N = 82) from different ethno-religious groups (Chaldeans, Orthodox Christians, and Muslims) to explore the potential risk and the protective factors associated with the high level of binge (or episodic heavy) drinking among Arab/Chaldeans reported by general population surveys. Most of the participants were aware of and knowledgeable about the problem in their community. Themes identified as contributory factors consistent across ethno-religious groups included the availability of alcohol, the importance of family, conformity to group behavior, and social reasons. Differences included the context for drinking and gender roles. These findings can be used to tailor culturally appropriate interventions.
Association between serum calcium and periodontal disease progression in non-institutionalized elderly.

OBJECTIVE To assess the effect of baseline serum calcium on the progression of periodontal disease in non-institutionalized elderly. BACKGROUND Although a few studies have found some evidence of the role played by dietary calcium in periodontal disease process, there is a paucity of information pertinent to longitudinal assessment of serum calcium-periodontal relationships. MATERIAL AND METHODS Clinical attachment levels of 266 Japanese subjects aged 70 years were recorded at baseline and annually for six consecutive years. Progression of periodontal disease (PPD) was defined as the number of teeth that showed additional attachment loss of > or =3 mm during the 6 years. The number of PPD was calculated for each subject and categorised into four levels, namely, PPD(0), PPD(1), PPD(2) and PPD(3) where the number of teeth with additional attachment loss ranged from 0, 1-10, 11-20 and >20 respectively. The levels of serum calcium, albumin, random blood sugar, immunoglobulin (IgG, IgA and IgM), gender, smoking habits, education, gingival bleeding and the number of teeth present were obtained at baseline. RESULTS Serum calcium, IgA, smoking, gingival bleeding and teeth present were associated with PPD at p < or = 0.10 and were included in a multinomial logistic regression analysis. Serum calcium was the only variable that was significantly associated with PPD with relative risks of 100 at PPD(1) and PPD(2), respectively, and 1000 at PPD(3). CONCLUSION Serum calcium may be considered a risk factor for periodontal disease progression in non-institutionalized elderly.
Early Results of Flexor Tendon Repair in Zone II With Modified, Four-Strand Strickland Technique

New materials, techniques of tendon suture and methods of post-operative rehabilitation offer surgeons perspective of effective repair and excellent outcomes. Results of experimental studies show that multistrand tendon suture provides better mechanical properties than two-strand technique, however, clinical use in only 4 studies did not confirm its definitive superiority to traditional method of the repair. the aim of the study was the assessment of the outcomes of the treatment of flexor tendon repair by a modified, four-strand Stickland technique. material and methods. Flexor tendons lacerations in 60 patients, all in Verdan’s zone II, without associated bone fractures and impaired blood supply were repaired by a modified, four-strand Stickland technique. An active flexion and extension of the fingers in the range restricted by a splint was recommended immediately after operation. Early results were evaluated in 51 patients, 41 men and 10 women, in a mean age of 31 years, in whom 69 tendons were repaired in 69 digits. Follow-up at 2 and 6 weeks included examination of total active range of motion (AROM) of involved fingers, rupture rate and complications. Results. Failure of the repair occurred in 3 cases (6%), including one thumb, index and little finger, all between 2nd and 6th week after the operation. A mean AROM at 2 and 6 weeks was 38% and 58% of the normal value (270° for the finger and for 170° the thumb), respectively. In 13 digits (28%) AROM at 6 weeks was excellent, greater than 80%, but in 5 digits was poor, less than 20% of the normal value. The main cause of reduced AROM was incomplete extension of the digits, due to splint employment up to 6 weeks post-operatively. conclusions. Early results obtained in the study fail to confirm greater endurance of four-strand repair over two-strand, what suggest rupture rate closed to given in the literature. An active range of motion achieved in the group was poorer than obtained after two-strand repair in other studies, but one can expect its improvement in the longer perspective. key words: flexor tendon repair, surgery POLSKI PRZEGLĄD CHIRURGICZNY 10.2478/v10035-008-0100-8 2008, 80, 12, 645–652
Supporting the Support System: How Assessment and Communication Can Help Patients and Their Support Systems

Purpose/Objective: The benefits of having a support system, such as social relationships with close friends and family, have been well documented for patients with serious health issues. As scientific evidence has shown, individuals who have the lowest level of involvement in social relationships face a greater mortality risk. Support systems, however, are not infallible. Relationship stress can have a negative impact on people—patient and caregiver alike—behaviorally, psychosocially, and physiologically. The purpose of this article is to encourage case managers who take a patient-centered approach to also consider the existence and extent of the support system, as well as any stresses or tensions that are observable within the support system. Although the case manager is ethically obliged to advocate for the individual receiving case management services, that advocacy can be extended to the support system for the good of all. Primary Practice Settings: This discussion applies to numerous case management practices and work settings including (but not limited to) hospital-based case management, home health, geriatrics, catastrophic case management, mental health, palliative care, and end of life/hospice. Finding/Conclusions: As part of the assessment phase of the case management process, case managers determine the extent of the patient's support system or social support network such as family and close friends. Although their advocacy is primarily for the patient receiving case management services, case managers also become aware of the needs of the support system members as they face their loved one's serious illness, severe injury, geriatric care demands, or end of life. Case managers can use their communication skills, especially motivational interviewing, with patients and their support systems to identify stresses and issues that can impact the pursuit of health goals. In addition, case managers ensure that individuals and their support systems are kept informed such as about the health condition, stage of disease, plan of care, treatment options, and care transition plan. Implications for Case Management: Professional case managers expand their role as advocates, serving primarily the patients (“clients”) who receive case management services and also members of the support system. By becoming more aware and sensitive to the needs of the support system, case managers help reduce stress on the support system, which can contribute to positive outcomes for patients (“clients”).
Maternal high‐fat feeding primes steatohepatitis in adult mice offspring, involving mitochondrial dysfunction and altered lipogenesis gene expression

Nonalcoholic fatty liver disease (NAFLD) describes an increasingly prevalent spectrum of liver disorders associated with obesity and metabolic syndrome. It is uncertain why steatosis occurs in some individuals, whereas nonalcoholic steatohepatitis (NASH) occurs in others. We have generated a novel mouse model to test our hypothesis: that maternal fat intake contributes to the development of NAFLD in adult offspring. Female mice were fed either a high‐fat (HF) or control chow (C) diet before and during gestation and lactation. Resulting offspring were fed either a C or a HF diet after weaning, to generate four offspring groups; HF/HF, HF/C, C/HF, C/C. At 15 weeks of age, liver histology was normal in both the C/C and HF/C offspring. Kleiner scoring showed that although the C/HF offspring developed nonalcoholic fatty liver, the HF/HF offspring developed NASH. At 30 weeks, histological analysis and Kleiner scoring showed that both the HF/C and C/HF groups had NAFLD, whereas the HF/HF had a more severe form of NASH. Therefore, exposure to a HF diet in utero and during lactation contributes toward NAFLD progression. We investigated the mechanisms by which this developmental priming is mediated. At 15 weeks of age, hepatic mitochondrial electron transport chain (ETC) enzyme complex activity (I, II/III, and IV) was reduced in both groups of offspring from HF‐fed mothers (HF/C and HF/HF). In addition, measurement of hepatic gene expression indicated that lipogenesis, oxidative stress, and inflammatory pathways were up‐regulated in the 15‐week‐old HF/C and HF/HF offspring. Conclusion: Maternal fat intake contributes toward the NAFLD progression in adult offspring, which is mediated through impaired hepatic mitochondrial metabolism and up‐regulated hepatic lipogenesis. (HEPATOLOGY 2009.)
Cytokine and chemokine expression in the skin from patients with maculopapular exanthema to drugs

Background: Maculopapular exanthema (MPE) is the most frequent clinical manifestation of nonimmediate allergic reactions to drugs and T helper 1 (Th1) cytokines and CD4+ T cells have been shown to play an important role in its pathogenesis. We assessed the role of cytokines and chemokines and their receptors in the pathogenesis of MPE.
Mouse organic solute transporter α deficiency enhances renal excretion of bile acids and attenuates cholestasis

Organic solute transporter alpha‐beta (Ostα‐Ostβ) is a heteromeric bile acid and sterol transporter that facilitates the enterohepatic and renal‐hepatic circulation of bile acids. Hepatic expression of this basolateral membrane protein is increased in cholestasis, presumably to facilitate removal of toxic bile acids from the liver. In this study, we show that the cholestatic phenotype induced by common bile duct ligation (BDL) is reduced in mice genetically deficient in Ostα. Although Ostα−/− mice have a smaller bile acid pool size, which could explain lower serum and hepatic levels of bile acids after BDL, gallbladder bilirubin and urinary bile acid concentrations were significantly greater in Ostα−/− BDL mice, suggesting additional alternative adaptive responses. Livers of Ostα−/− mice had higher messenger RNA levels of constitutive androstane receptor (Car) than wild‐type BDL mice and increased expression of Phase I enzymes (Cyp7a1, Cyp2b10, Cyp3a11), Phase II enzymes (Sult2a1, Ugt1a1), and Phase III transporters (Mrp2, Mrp3). Following BDL, the bile acid pool size increased in Ostα−/− mice and protein levels for the hepatic basolateral membrane export transporters, multidrug resistance‐associated protein 3 (Mrp3) and Mrp4, and for the apical bilirubin transporter, Mrp2, were all increased. In the kidney of Ostα−/− mice after BDL, the apical bile acid uptake transporter Asbt is further reduced, whereas the apical export transporters Mrp2 and Mrp4 are increased, resulting in a significant increase in urinary bile acid excretion. Conclusion: These findings indicate that loss of Ostα provides protection from liver injury in obstructive cholestasis through adaptive responses in both the kidney and liver that enhance clearance of bile acids into urine and through detoxification pathways most likely mediated by the nuclear receptor Car. (HEPATOLOGY 2010.)
High altitude medicine and physiology.

Clinical risk management is a strange subject which will perplex many readers. If this was a book about cricket, it would have chapters on no balls, wides, missed stumpings, and accusations by Indian bookmakers, but it probably would not talk about how to be a successful cricketer. As a result, some readers will be a bit put off by both its lay out and content. However, for those …
Increased caffeine consumption is associated with reduced hepatic fibrosis

Although coffee consumption has been associated with reduced frequency of liver disease, it is unclear whether the effect is from coffee or caffeine and whether there is an effect on hepatic fibrosis specifically. This study was undertaken to use a food‐frequency instrument for dietary caffeine consumption to evaluate the relationship between caffeine intake and liver fibrosis. Patients undergoing liver biopsy completed a detailed caffeine questionnaire on three occasions over a 6‐month period. Caffeine intake was compared between patients with mild and advanced liver fibrosis (bridging fibrosis/cirrhosis). Logistic regression was used to evaluate the association between caffeine consumption and hepatic fibrosis. One hundred seventy‐seven patients (99 male, 104 white, 121 with chronic hepatitis C virus [HCV] infection) undergoing liver biopsy completed the caffeine questionnaire on up to three occasions. Results from repeated questionnaires were consistent. Daily caffeine consumption above the 75th percentile for the cohort (308 mg = approximately 2.25 cups of coffee equivalents) was associated with reduced liver fibrosis (odds ratio [OR], 0.33; 95% confidence interval [CI], 0.14‐0.80; P = 0.015) and the protective association persisted after controlling for age, sex, race, liver disease, body mass index, and alcohol intake in all patients (OR, 0.25; 95% CI, 0.09‐0.67; P = 0.006), as well as the subset with HCV infection (OR, 0.19; 95% CI, 0.05‐0.66; P = 0.009). Despite a modest trend, consumption of caffeine from sources other than coffee or of decaffeinated coffee was not associated with reduced liver fibrosis. A reliable tool for measurement of caffeine consumption demonstrated that caffeine consumption, particularly from regular coffee, above a threshold of approximately 2 coffee‐cup equivalents per day, was associated with less severe hepatic fibrosis. (HEPATOLOGY 2010;51:201–209.)
Systematic review of randomized trials on vasoconstrictor drugs for hepatorenal syndrome

Vasoconstrictor drugs may improve renal function in hepatorenal syndrome (HRS), but the effect on mortality has not been established. We therefore performed a systematic review of randomized trials on vasoconstrictor drugs for type 1 or type 2 HRS. Mortality was the primary outcome measure. Eligible trials were identified through electronic and manual searches. Intention‐to‐treat random effects meta‐analyses were performed. Ten randomized trials on terlipressin alone or with albumin, octreotide plus albumin, and noradrenalin plus albumin were included. The total number of patients was 376. Overall, vasoconstrictor drugs used alone or with albumin reduced mortality compared with no intervention or albumin (relative risk [RR], 0.82; 95% confidence interval [CI], 0.70–0.96). In subgroup analyses, the effect on mortality was seen at 15 days (RR, 0.60; 95% CI, 0.37–0.97) but not at 30 days (RR, 0.74; 95% CI, 0.40–1.39), 90 days (RR, 0.89; 95% CI, 0.66–1.22), or 180 days (RR, 0.83; 95% CI, 0.65–1.05). Subgroup analyses stratified by the treatments assessed showed that terlipressin plus albumin reduced mortality compared with albumin (RR, 0.81; 95% CI, 0.68–0.97). The effect was seen in subgroup analyses of type 1 but not type 2 HRS. The remaining trials were small and found no beneficial or harmful effects of the treatments assessed. Conclusion: Terlipressin plus albumin may prolong short‐term survival in type 1 HRS. The duration of the response should be considered when making treatment decisions and in the timing of potential liver transplantations. Considering the small number of patients included, the evidence does not allow for treatment recommendations regarding type 2 HRS or any of the remaining treatment comparisons assessed. (HEPATOLOGY 2009.)