Tag Archives: casr

In this paper we present a heterodox open economy

In this paper we present a heterodox open-economy macroeconomic model that seeks to establish an alternative view to the “New Consensus” model and analyze the determinants of long-run inflation, the transmission casr of monetary policy, the costs of such policy and its limitations. The structure of the model intends to be simple, in order to be comparable to the new consensus model. We will analyze an open-economy were inflation is a cost-push phenomenon and the monetary authority can manage the nominal exchange rate through changes in interest rate differentials. In this model we will incorporate an explicit inflation target regime in the sraffian supermultiplier model in order to analyze how economic policy can influence the growth rate of productive capacity and the Functional income distribution.

An alternative model to the open-economy “new consensus”

The model closure and analytical solution
To close our model we need to establish how the interest rate is determined. We suppose, as in the new consensus model, that the monetary authority set the nominal interest rate in order to achieve inflation target (π). The Monetary Authority raises the nominal interest rate when inflation is above target, and lowers when it is below:
In order to obtain the analytical solution, we depart from the Phillips curve (Equation 14). The long run inflation will depend on the permanent pressures on inflation. Demand shocks, as we discuss, are temporary as the productive capacity adjusts to the current output level. In the long run, this source of pressure disappears. Cost-push shocks such as changes in nominal interest rates (Δi) are also temporary, since there is a nominal interest rate (i=i) that is capable of achieving inflation target. So, in the long run we do not expect changes in the nominal interest rate.
Consequently, in the long run, inflation will depend on international inflation, changes in nominal exchange rate, on the degree of distributive conflict “c” and on the inflation inertia degree:
We have the following system to solve:
From Eq. (24) we can deduce that, given international inflation, the share of imported inputs, inflation inertia degree and workers’ bargaining power c, there is a change in nominal exchange rate that can bring long run inflation to the target.
To achieve this exchange rate change, the monetary authority must set domestic interest rate above international rate. We will denote the domestic interest rate necessary to change nominal exchange rate and thus to bring long run inflation to the target as (i). Replacing Eq. (24) in (22) and as if π=π→i=i, we have:
Thus, the domestic interest rate necessary to change nominal exchange rate and thus to bring long run inflation to the target (i) will be:
As we can see, there is an inverse relation between nominal interest rates and the inflation target. The slope of this relation depends on the inflation inertia degree “a”, m* and l*c, while the position depends on international conditions (πw, (iw+ρ), F′/δ).
Replacing i and π in Eq. (6) we find the growth rate of autonomous expenditures (z)
Eq. (27) shows us that there is a positive relation between the growth rate of autonomous spending (z) and inflation target. So, the higher is inflation target, the higher will be growth rate of the growth rate of autonomous spending.
Finally, the growth rate of productive capacity will be the result of both autonomous spending and the multiplier, whith the latter changing as consequence of variations in functional income distribution, according to Eq. (9) and (15).

Numerical simulations
In the numerical simulation exercise, the extreme hypothesis of h=1 in the adaptive exchange rate expectation (20) is abandoned and the exchange rate expectations now depends on an average weight of past exchange rate.
The initial condition, parameters and exogenous variables supposed are: (a) inflation starts at 6%; (b) First exchange rate expectations is 4,0 and the parameter h is 0,76; (c) International interest rate is 5% and sovereign spread is 2%; (d) initial domestic nominal interest rate is 20%; (d) Output and productive capacity initial levels are in equilibrium and are equal to 400; (e) Exogenous component of growth rate of autonomous expenditures, σ is 8%; (f) The monetary authority\’s rule parameter γ is 0,7; (g) a high value of δ, denoting that short run capital flows are highly sensitive to interest rate differentials. All the simulations start with the same initial conditions.

A key mechanism whereby macrophages may

A key mechanism whereby macrophages may affect tissue repair and regeneration is by instructing the stem cell niche by paracrine mechanisms. In the mouse skeletal muscle injury model, macrophage-derived paracrine factors promote satellite cell survival, proliferation and differentiation in vitro and in vivo (Cantini et al., 1994; Chazaud et al., 2003). In the mouse hepatic injury model, phagocytic macrophages activate HPCs via Wnt3a signalling, to induce HSP proliferation and differentiation (Boulter et al., 2012). Depletion of macrophages sharing the HPC niche results in re-specification of HPCs to generate peri-portal biliary structures instead of hepatocytes (Boulter et al., 2012).
Macrophages also occupy the haematopoietic stem cell (HSC) niche (Chow et al., 2011b; Ludin et al., 2012; Winkler et al., 2010). Macrophage depletion using either Clo-Lip, macrophage-specific genetic or antibody-mediated depletion strategies, results in egression of haematopoietic stem casr (HSCs). Here, also, paracrine signalling is important with Cxcl12 playing a prominent role (Chow et al., 2011b; Ludin et al., 2012; Winkler et al., 2010; Christopher et al., 2011). Depletion of bone marrow macrophages leads to a significant decrease in Cxcl12 production (Chow et al., 2011b; Ludin et al., 2012; Winkler et al., 2010; Christopher et al., 2011), a critical factor for HSC homeostasis (Sugiyama et al., 2006). Moreover, macrophage G-CSFR is important for regulation of Cxcl12 and HSC mobilisation, with macrophage-restricted G-CSFR expression sufficient for G-CSF mediated HSC egression (Christopher et al., 2011). These observations indicate that macrophages, in particular subepicardial cTMs, may act as gatekeepers regulating progenitor cell mobilisation.
Macrophages likewise positively regulate mesenchymal stem cells. In vitro experiments on cultured human MSCs demonstrate that macrophage-derived growth factors enhance MSC growth, viability, motility and secretion of paracrine factors (Freytes et al., 2013; Anton et al., 2012). MSC mobilising factors include IL-8, Mcp-1 and CCL5, which are chemotactic for MSCs (Anton et al., 2012). However, macrophage-MSC interactions are not uni-directional. MSCs transplanted to the injured myocardium induce a shift in the balance of macrophages to an M2-like phenotype (Ben-Mordechai et al., 2013). Similarly, in a spinal cord injury model, MSC transplantation shifts macrophage phenotype to an M2-like phenotype, leading to improved functional recovery (Nakajima et al., 2012). These findings are consistent with in vitro evidence that supernatants from cultured human MSCs polarise human monocyte-derived macrophages towards M2-like cells (Kim & Hematti, 2009).
Finally, macrophages play a significant role in promoting cancer stem cell proliferation and activation (De Palma & Lewis, 2013). Tumour associated macrophages (TAMs), closely resembling M2 macrophages (Pucci et al., 2009; Mantovani et al., 2002), release a number of paracrine factors that regulate cancer stem cells (CSCs) (De Palma & Lewis, 2013), including those that induce tumour cells to acquire cancer stem cell-like phenotypes (Yang et al., 2013; Jinushi et al., 2011). Depletion of macrophages by either using Clo-Lip or synthetic inhibitors of macrophage colony stimulating factor 1 receptor results in a reduction in the number and activity of CSCs within tumours and increased sensitivity to chemotherapeutic agents (Yang et al., 2013; Mitchem et al., 2013). Taken together, these examples underscore the importance of macrophage-stem cell cross talk for stem cell homeostasis and mobilisation. Considering the close interaction of cTMs with the epicardium (Pinto et al., 2014), these observations indicate that cTMs may be important for epicardial progenitor cell homeostasis and potential maintenance of the progenitor cell phenotype.

Challenges and future perspectives
While a significant body of work indicates that macrophages are critical for tissue homeostasis, repair and regeneration, much work is still required to delineate the precise contribution of macrophages in these processes particularly in the heart. Indeed, recent work has demonstrated that the regeneration of the mouse neonatal heart and adult axolotl heart is dependent on macrophages (Aurora et al., 2014; Godwin, Pinto, Rosenthal, unpublished data). However, the basic questions of whether macrophages are merely required for clearance of tissue debris, an essential pre-requisite process for tissue injury resolution, or whether they play a greater role in directing cell fate and organogenesis remain to be unequivocally demonstrated.

Introduction Lead is a naturally occurring bluish

Lead is a naturally occurring bluish-gray metal found in small amounts in the Earth’s crust and can be found in all parts of our environment (Gupta, 2007). Lead is found in our food, water, air and soil. Lead emitted by smelters and boilers that burn used motor oil is frequently deposited in the soil, where it is taken up by crops (Chiras, 2009). Lead is known as an enzymatic toxicant, is neurotoxic, hemato and cardiovascular toxic, nephrotoxic, immunotoxic, carcinogenic, teratogenic and mutagenic (Kiran et al., 2009; Moreira and Moreira, 2004). Lead damages cellular materials, alters cellular genetics and produces oxidative damage. It causes hyperproduction of free radicals and decreased availability of anti oxidant reserves to respond to the resultant damage. It also interrupts enzyme activation and competitively casr inhibits trace mineral absorption. Lead binds to sulfhydryl proteins (interrupting structural protein synthesis), alters calcium homeostasis and lowers the levels of available sulfhydryl antioxidant reserves in the body (Lynpatrick, 2006). The toxicity of lead is closely related to age, sex, route of exposure level of intake, solubility, metal oxidation state, retention percentage, duration of exposure, frequency of intake, casr rate, mechanisms and efficiency of excretion. Lead has been associated with various forms of cancer, nephrotoxicity, central nervous system effects and cardiovascular diseases in humans (Pitot and Dragan, 1996).
Captopril (D-3-mercapto-2-methyl-propanoyl-L-proline) is an angiotension-converting enzyme (ACE) inhibitor. Besides, its role as a treatment for hypertension (Sultana et al., 2007), it is commonly used as a cardioprotective drug (Khattab et al., 2005). Like other ACE inhibitors, captopril inhibits the conversion of angiotensin I, a relatively inactive molecule, to angiotensin II which is the major mediator of vasoconstriction and volume expansion induced by the renin–angiotensin system. Captopril, an inhibitor of angiotensin converting enzyme (ACE), has also been postulated as a free radical scavenger because of its terminal sulfhydryl group (Bagchi et al., 1989; Andreoli, 1993). Some in vitro studies indicate that captopril functions as an antioxidant both by scavenging ROS and by increasing the activities of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase (Westlin and Mullane, 1988; Kojsova et al., 2006). Captopril has been shown to decrease serum lipid peroxide concentrations in diabetic patients (Ha and Kim, 1992).

Material and methods


Lead had been a toxic problem for human beings from the earliest time. The ingested and absorbed lead stored primarily in soft tissues and bone, but the highest concentration of lead occurs within the bone, teeth, liver, lung, kidney, brain and spleen (Plumlee, 2004; Mudipalli, 2007). The present study resulted in insignificant differences in liver and spleen indices between control and experimental lead groups, that run in agreement with (Allouche et al., 2011). Histological investigations revealed that lead acetate exposure resulted in marked changes in the liver these findings agreed with (Jankeer and El-Nouri, 2009; Muselin et al., 2010; Suradkar et al., 2010) they stated that rat exposure to lead acetate caused hepatotoxicity characterized by engorgement of blood vessels along with sinusoidal hemorrhage, infiltration, dilatation of central veins and vacuolar degeneration of hepatocytes. In the present study, lead reached the liver via the portal vein that the liver is the first organ exposed to internally absorbed nutrients and other xenobiotics so lead accumulated in the liver tissue caused severe alterations characterized by congested and dilated portal veins and degeneration in hepatic cells with moderate ballooning, severe inflammation, apoptotic cells and mild fibrosis. Most orally ingested lead is excreted, but a portion is absorbed and is transferred to the blood where lead binds to hemoglobin in the erythrocytes so lead is carried through the circulatory system by erythrocytes, virtually all tissues in the body can become exposed to the toxic metal, particularly hematopoietic and immune system (Goering, 1993; Gidlow, 2004; Lawrence and McCabe, 1995). In the spleen, phagocytes (macrophages and polymorphonuclear cells) are responsible for slowing the propagation of an invading pathogen, while an antigen-specific adaptive immune response (antibody- or cell-mediated) is being established. Lead was reported to inhibit macrophage function (Kowolenko et al., l988; Mauel et al., 1989) possibly by overloading macrophages with cellular debris and inhibiting macrophage production of nitric oxide (Tian and Lawrence, 1995). In the context of adaptive humoral and cellular immune responses, lead increased both B-cell and T-cell in vitro proliferation (Lawrence, 1981a–c; Warner and Lawrence, 1986; Razani et al., 1999). In the present study, administration of lead resulted in severe changes in the spleen represented by severe lymphoid necrosis, moderate diffusion of white pulp into the red pulp, diminished lymphoid follicles and appearance of large macrophages might be due to the production of debris of dead cells.

Subjects were within young age group

Subjects were within young age group. Advancement in age decreased sperm count and motility. Subjects belonged to a limited geographical area. Fernandez et al. reported quality of semen differed among people from place to place.
More number of days of abstinence deteriorated semen quality. We advised 2–5days abstinence which was necessary to get normal semen and others advised 0 to 2–7days. Studies had shown the difference in quality of semen in daily and in more frequent ejaculation. Frequency of collection was having a significant effect on the composition of semen, with respect to volume, sperm density, seminal plasma constituents and other parameters.
Mode of collection of sample was masturbation. Coitus interruptus was not advised due to chances of losing one or two drops during collection as well as mixing the sample with vaginal secretions and vaginal cells. Total semen was important for the study. Also portion of semen differed in total sperm count and pattern of its motility.
Providing a place next to laboratory for sample collection suited not to damage sperms during the transition casr caused by movement as well as change in temperature and to learn sample from almost collection time. Others also opted for similar way. In this study, liquefaction time was below 15min. Sample collected at different places required minimum 30min to 1h even more time to submit it to laboratory. Sperm motility decreased with slight change in biophysical condition and also deteriorated as time lapsed. We studied sperm motility from 30m after collection (Table 1). Others advised to perform within 1h or 2–4hm.
We provided wide mouthed container for collection which permitted not to lose any drop. Each portion of semen differed. Semen collected in narrow mouthed bottle or test tube may lead to missing a small portion of sample. Well cleaned containers supplied were to exclude unknown chemicals possibly present in containers otherwise used. For the same reason condom was not suitable for collection of sample as which was known to contain chemicals.
Devices for semen collection were designed and discussed by different authors. All type of containers were not suitable for storage of sample used for chemical study.
Subjects collected sample at 8am (±30m). Statistically significant difference in semen quality was observed when samples were collected at different timings of the day. Similar chronobiological changes in body was known. Present study was restricted to one month period. Singh et al. reported seasonal changes in semen electrolytes.
Veena et al. had shown sperm motility was better in dark than in light. Considering this, we maintained constant wave length of light in laboratory and a fixed level of light on stage of microscope throughout our study. The importance of sample and the slide to remain near 37°C while for studying sperm motility was taken care following Freund. The effect of temperature in samples was known since 1962. Semen study was carried out as per WHO. A minimum amount of antibiotics was added to sample as it was known that seminal plasma was not a good medium for sperm survival.
Total semen volume, liquefaction time, pH and test for presence of fructose were within normal range. Total sperm count and percentage of total, PR and NP motility were also within normal range (Table 1).
One of the two aspects of present study was on sperm motility. Percentage of sperm motility was significantly correlated with total sperm count. Results on total sperm motility (%) showed a fall in it from 75.6±3.22 (1/2h) to 9.8±2.77 (24h). Percentage of total motility was decreasing from 1h of study though statistically significant difference (<0.01) was seen from 2h. Significant fall (<0.01) was seen in PR motile sperms from 1h (Table 2). Eliasson and Freund observed a significant correlation between sperm motility and rate of forward progressing motile sperms. Number of NP sperms increased from 1h (<0.05) to 4h. time, compensating the fall in PR (Table 1). Our study was likely to be the first one of its kind to show that total sperm motility was >50% at 8h. after ejaculation (Table 1 and Fig. 1). Normally, the overall motility reached a minimum of 60 percentage after 2–3h of ejaculation. A significant decrease in sperm motility over 2–4h period indicated a serious problem even if the sperm count and original motility were good. One reason for decrease in sperm motility was due to the change in organic and inorganic elements. Sperm motility inhibitory factors present in semen were also responsible which were removed from semen after its deposition in vagina.