The sequence of action for performing mouth to mouth and nose breaths for an infant is by blowing a breath steadily into the mouth of baby and nose only for a second.
It is necessary to make the additional breathe and make chest rise. Firstly, take a breathe and cover baby's mouth and nose with the mouth and blow the air into nose. Chest pressing can also done if the mouth to mouth action is not working. It also helps in gaining the breathe to an infant.
By rubbing the hands and foot of an infant produces heat to the infant's body and helps in breathing.
Chest pressing is the process of gaining the breathe or make the person breathe by pressing the chest.
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Answer:
Obesity is a major contributor to the burden of metabolic dysfunction and to several chronic diseases including type 2 diabetes [1]. In the southern parts of Ghana, especially in the Greater Accra region and its environs, the prevalence of obesity and type 2 diabetes have been reported to be increasing steadily [2, 16]. What is not clear is the contributory effects of gender, physical activity and diabetes mellitus on obesity. The present study evaluated the impact of serum leptin and hsCRP levels in obese Ghanaian subjects with and/or without type 2 diabetes. In this study, obese subjects with type 2 diabetes had lower serum leptin but higher hsCRP concentrations than obese non-diabetic individuals. Multivariate analysis further revealed that, obese persons with type 2 diabetes were three times less likely to have elevated leptin levels than obese controls. Further, obese diabetic men in this study, with poor glycemic control, had lower leptin levels. A possible explanation for reduced leptin levels in persons with type 2 diabetes may be due to insulin resistance, a modulator of leptin production. Thus defect in glucose sensing, as seen in type 2 diabetes could be responsible for the lower leptin production, suggesting a signalling crosstalk in glucose regulation. Altered body fat distribution in diabetic subjects have been suggested as an alternative explanation for lowered leptin levels [17,18,19,20]. Even though this study did not observe differences in visceral fat among the two groups, leptin levels correlated positively with measures of adiposity and body composition in both groups indicating a possible synergistic effect. A third explanation could be due to the use of statin medications. Twelve (12) of our case subjects were on lipid lowering drugs and this could have contributed to such an observation. Result however were not statistically significantly when we excluded those on lipid lowering drugs from the analysis. Serum leptin levels in this study was also influenced by gender. Obese females were about 10 times more likely to have higher leptin levels than obese males. Stimulation of leptin mRNA production by 17β-estradiol in females could explain the above observation [21]. An inverse relationship has also been observed in a male cohort for leptin versus testosterone levels [22]. Levels of hsCRP among obese persons with type 2 diabetes in this study, was significantly higher than controls suggesting a possible directional relationship between insulin resistance and chronic inflammation. Whereas this study showed no variations in body composition, prior studies showed a strong association between hsCRP and measures of central obesity [23]. In summary, results highlight relationships of leptin and hsCRP with obesity and type 2 diabetes. We demonstrated that type 2 diabetes and gender were independent factors in determining serum leptin levels among obese subjects.
A young woman’s first menstrual period is known as <span>menarche.</span>
