Breast Feeding Practices among Families of Armed Forces Personnel in a Large Cantonment

Background

There seems to be a gap in the available literature and scientific knowledge about breast-feeding practices among families of armed forces personnel in our country, which needs to be studied.

Methods

A cross sectional epidemiological study design was undertaken on a randomly selected sample of 175 families of armed forces personnel staying in a large cantonment and having at least one child in the age group of 3–24 months.

Result

The study observed positive association between various breast feeding practices such as feeding colostrum, demand/scheduled feeding, exclusive breast feeding for 4–6 months, partial breast feeding for 6 – 18 months and various sociodemographic variables such as age, religion, socio-economic status of mother (military rank of husband), parity and place of residence of the mother (where childhood was spent).

Conclusion

Higher proportion of mothers feeding colostrum was observed because of better educational status of mothers and organized health education activities available to the families of armed forces personnel. Majority (89.14%) gave demand feed and only 10.86% gave scheduled feed. On the other hand a relatively smaller percentage (47.43% and 29.32%) followed the correct practice about duration of exclusive and partial breast-feeding respectively.Key Words: Colostrum, Demand/Scheduled feeding, Breast feeding     

Diet,MicroRNAs and Prostate Cancer

MicroRNAs (miRNAs) constitute an evolutionarily conserved class of small non-coding RNAs that are endogenously expressed with crucial functions in fundamental cellular processes such as cell cycle, apoptosis and differentiation. Disturbance of miRNA expression and function leads to deregulation of basic cellular processes leading to tumorigenesis. A growing body of experimental evidence suggests that human tumors have deregulated expression of microRNAs, which have been proposed as novel oncogenes or tumor suppressors. Recent studies have shown that microRNA expression patterns serve as phenotypic signatures of different cancers and could be used as diagnostic, prognostic and therapeutic tools. A few studies have analyzed global microRNA expression profiles or the functional role of microRNAs in prostate cancer. Here we have reviewed the role of microRNAs in prostate carcinogenesis by summarizing the findings from such studies. In addition, recent evidence indicates that dietary factors play an important role in the process of carcinogenesis through modulation of miRNA expression, though such studies are lacking in regards to prostate cancer. It has been proposed that dietary modulation of miRNA expression may contribute to the cancer-protective effects of dietary components. In this review, we have summarized findings from studies on the effect of dietary agents on miRNA expression and function.     

DNA mismatch repair gene MLH1 induces apoptosis in prostate cancer cells

Mismatch repair (MMR) enzymes have been shown to be deficient in prostate cancer (PCa). MMR can influence the regulation of tumor development in various cancers but their role on PCa has not been investigated. The aim of the present study was to determine the functional effects of the mutL-homolog 1 (MLH1) gene on growth of PCa cells. The DU145 cell line has been established as MLH1-deficient and thus, this cell line was utilized to determine effects of MLH1 by gene expression. Lack of MLH1 protein expression was confirmed by Western blotting in DU145 cells whereas levels were high in normal PWR-1E and RWPE-1 prostatic cells. MLH1-expressing stable transfectant DU145 cells were then created to characterize the effects this MMR gene has on various growth properties. Expression of MLH1 resulted in decreased cell proliferation, migration and invasion properties. Lack of cell growth in vivo also indicated a tumor suppressive effect by MLH1. Interestingly, MLH1 caused an increase in apoptosis along with phosphorylated c-Abl, and treatment with MLH1 siRNAs countered this effect. Furthermore, inhibition of c-Abl with STI571 also abrogated the effect on apoptosis caused by MLH1. These results demonstrate MLH1 protects against PCa development by inducing c-Abl-mediated apoptosis.     

Killip classification in patients with acute coronary syndrome: insight from a multicenter registry

The purpose of this study was to assess the prognostic value of the Killip classification at the presentation in patients with acute coronary syndrome (ACS). In 2007 and over 5 months, 6704 consecutive patients with ACS were enrolled in the Gulf Registry of Acute Coronary Events. Patients were categorized according to Killip classification at presentation (Classes I, II, III, and IV). Patients' characteristics and in-hospital outcomes were analyzed. High Killip classes were defined in 22% of patients. In comparison to Killip Class I, patients with higher Killip class had greater prevalence of cardiovascular risk factors, presented late, were less likely to have angina, and were less likely to receive antiplatelet, statins, and β-blockers. Classes II, III, and IV were associated with higher adjusted odds of death in ST-elevation myocardial infarction (odds ratio [OR] 2.1, 95% confidence interval [CI] 1.25-3.69; OR 6.1, 95% CI 3.41-10.86; and OR 28, 95% CI 15.24-54.70, respectively) and non-ST-elevation acute coronary syndrome (adjusted OR 2.4, 95% CI 1.24-4.82; OR 3.2,95% 1.49-7.02; and OR 9.8, 95% CI 3.79-25.57, respectively). In conclusion, across ACS, patients with higher Killip class had worse clinical profile and were less likely to be treated with evidence-based therapy. High Killip class was independent predictors of mortality in ST-elevation myocardial infarction and non-ST-elevation acute coronary syndrome. Physician in the emergency department should be aware of the importance of clinical examination in the risk stratification in patients presenting with ACS.     

DICKKOPF-4 activates the noncanonical c-Jun-NH2 kinase signaling pathway while inhibiting the Wnt-canonical pathway in human renal cell carcinoma

BACKGROUND:

To the authors' knowledge, the functional significance of the Wnt antagonist dickkopf homolog 4 (DKK4) has not been investigated previously in renal cancer.

METHODS:

The authors initially observed that the expression of DKK4 was significantly higher in renal cancer tissues compared with adjacent normal kidney tissues. To assess the function of DKK4, stable DKK4‐transfected cells were established, and functional analyses were performed, including a T‐cell factor/lymphoid enhancer factor (TCF/LEF) reporter assay and tests for cell viability, colony formation, apoptosis, cell cycle, invasive capability, wound‐healing capability, and in vivo tumor growth.

RESULTS:

The relative TCF/LEF activity was significantly lower in DKK4‐transfected cells compared with empty vector, and nuclear β‐catenin expression was decreased in DKK4 transfectants. In addition, expression levels of the β‐catenin downstream effector proteins cyclin D1 and c‐Myc were decreased in DKK4 transfectants. However, greater invasiveness and migration were observed in stably transfected DKK4 cells. Increased growth of DKK4‐transfected tumors also was observed in nude mice. Members of the Wnt noncanonical/c‐Jun‐NH2 kinase (JNK) signaling pathway also were effected, such as c‐Jun, which had significantly increased expression and phosphorylation in DKK4‐stable transfectants, and matrix metalloproteinase‐2, which had significantly increased expression in DKK4‐stable transfectants.

CONCLUSIONS:

This is the first study to indicate that DKK4 expression is increased in renal cancer tissues and that DKK4 activates the noncanonical JNK signaling pathway while inhibiting the Wnt‐canonical pathway. Cancer 2011. © 2010 American Cancer Society.