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Carcinoembryonic Antigen Linked Mobile Adhesion Molecule Half a dozen Stimulates Carcinogenesis regarding Abdominal Cancer and also Anti-CEACAM6 Luminescent Probe Could Analyze the Precancerous Lesions.
Loss of cardiomyocytes due to apoptotic or necrotic death is an important component of the pathogenesis of heart failure. Initiation of apoptosis by the mitochondrial pathway depends on the balance between proapoptotic and antiapoptotic factors, in particular, Bax and Bcl-2. Cardiomyocyte apoptosis in essential hypertension is studied in sufficient details. At the same time, apoptotic processes in the myocardium in diabetes mellitus alone and in combination with essential hypertension remain poorly understood. Here we studied the expression of Bax and Bcl-2 in the left ventricular cardiomyocytes of 38-week-old male Wistar-Kyoto rats and 38- and 57-week-old SHR rats with essential hypertension, diabetes mellitus, and a combination of these pathologies. Insulin-dependent diabetes mellitus was modelled by a single parenteral administration of streptozotocin in a dose 65 mg/kg. Expression of Bax and Bcl-2 was assessed by the immunohistochemical method. In essential hypertension and diabetes mellitus, the apoptotic processes in the ventricular myocardium were enhanced, as is seen from the increase in the content of the proapoptotic factor Bax and a decrease in the expression of the antiapoptotic factor Bcl-2. However, in case of combined pathology, Bax content increased less markedly, while the expression of antiapoptotic Bcl-2 was significantly increased.We studied electrophysiological changes in rabbit esophageal epithelium following acute (AS) and chronic stress (CS). Esophageal tissue was placed in Ussing chamber and the potential difference U between the luminal and abluminal sides, the short-circuit current Isc, as well as the tissue resistance R were measured. The initial values of these parameters for each sample were determined after the samples were stabilized in Ringer solution. Then, the tissues were exposed for 1 h to normal Ringer solution or Ringer solution with pH 4.0 and pH 1.7 with or without pepsin (0.25 mg/ml). Fluorescein was added to the luminal side of the sample to measure its permeability. In the AS group, U at Ringer solution (pH 1.7)+pepsin was significantly decreased in comparison with the baseline and control values (by 46 and 22%, respectively, p less then 0.05). R decreased by 74% in comparison with baseline, which little differed from the decrease in control samples exposed to Ringer solution (pH 1.7)+pepsin (by 62%). CS did not change U relative to baseline values, while changes in R were similar to those in the AS group. In the AS group, the permeability of the esophageal tissue perfused with Ringer solution (pH 1.7)+pepsin was significantly higher than in both the control and CS groups. AS, but not CS, made the esophageal epithelium more sensitive to the effects of noxious agents, disrupted barrier properties, and increased permeability. The effects of stress on gastroesophageal reflux disease symptoms can be related to severe exposure to acid and/or pepsin; however, the mechanisms other than epithelial defense should be evaluated.We studied the effect of CCK-8 on BP and blood content of CGRP in rats with hypertension caused by fructose or inhibition of NO synthase with L-NAME. The decrease in the CGRP content was found during the development of fructose-induced hypertension, but not L-NAME-caused hypertension. Administration of CCK-8 to fructose-fed animals reduced BP and increased the content of CGRP. In rats with hypertension caused by NO deficit, CCK-8 lowered BP, but did not affect the content of CGRP. These findings suggest that CGRP mediates the hypotensive effect of CCK-8 in fructose-induced hypertension, but not in NO-deficient hypertension.The study employed a rat model to examine the effects of taurine (Tau) on prevention and therapy of non-alcoholic fatty liver disease (NAFLD). In model rats maintained on a high-fat diet (HFD), the serum levels of ALT, AST, triglycerides, cholesterol, and LDL were higher than the corresponding levels in normal control and NP groups (p less then 0.05). this website In Tau-prevention and Tau-treatment groups, the serum levels of AST and triglycerides were lower than in HFD rats (p less then 0.05). In HFD rats, diffuse fatty degeneration and infiltration with inflammatory cells was observed in the liver; in the ileal mucosa, the villi were fractured or absent, the epithelium was exfoliated and infiltrated with inflammatory cells. The levels of TGF-β, IL-9, and their mRNA in the liver and ileal mucosa of HFD rats were significantly higher than in normal control and NP groups (p less then 0.05). In Tau-prevention and Tau-treatment groups, these levels were significantly lower than in HFD rats (p less then 0.05). Thus, TGF-β and IL-9 can be implicated in NAFLD genesis, while Tau can preventively or therapeutically diminish the damage to the liver and ileal mucosa in rats with this disease by down-regulating the expression of TGF-β and IL-9.In a relatively isolated system of avian embryo, the metabolism of NO, a component of the dinitrosyl iron complexes (DNIC), the main NO donor in most tissues, depends on the ligands that make up the complex. This fact corroborates the earlier hypothesis that these ligands perform a regulatory function in NO metabolism. It is also shown that nitrite injected into the embryo is not oxidized to nitrate like NO in DNIC, but is accumulated outside the amniotic sac. Normally, nitrite is present in an embryo in trace amounts. These facts suggest that NO in the embryo is transferred from the donor molecule to a target in the embryo tissues further transformed with minimum oxidation to nitrite.We studied the antioxidant and cytoprotective effects of meconic acid in the model systems. Meconic acid, similar to commercial drug Mexidol, reduced the intensity of chemiluminescence in the model system of yolk lipoproteins. Meconic acid also reduced the toxic effect of glutamate on neurons in the primary cerebellar culture, but had no effect on cell viability under normal conditions.The rhythmic variations of body temperature in two groups of mice located in Moscow and Novosibirsk were compared with geomagnetic undulations within Pc5/Pi3 (1-5 mHz) range measured in Borok and Novosibirsk middle-latitude geophysical observatories located at the same longitudes as the examined mice. The spectral maxima of geomagnetic undulations and body temperature variations were observed with greatest probability at the frequencies of 1.6, 2.3, and 3.1 mHz. At this, the mean square of the distance between the frequencies of spectral maxima of simultaneous oscillations was smaller than that of random intervals favoring the hypothesis on geomagnetic undulations as the synchronizer of biorhythms. In both groups of mice, the share of intervals with a high spectral coherency between geomagnetic undulations and body temperature variations had common maximum in the pre-midnight sector of local time and it was higher for the large-scale geomagnetic undulations. Dependence of geomagnetic undulations on spatial scale suggests that body temperature is affected by electrotelluric field.We studied the localization and severity of morphological changes in CNS and internal organs of animals intacerebrally infected with a low-attenuated rubella virus strain "Orlov-14". The data obtained can be used as morphological criteria reflecting low level of attenuation of rubella virus strains to improve the control of the safety of attenuated strains of live rubella vaccines.The role of stable hydrogen isotopes in the thermoregulation and its regulation is poorly studied. We analyzed fluctuations in body temperature and changes in thermoregulation parameters in mice under conditions of reduced deuterium intake. The study was performed on male C57BL/6 mice that consumed water with a low (10 ppm) and normal (146 ppm) deuterium content. In 7 days, fluctuations of body temperature, locomotor activity, and oxygen uptake were assessed. Deuterium depletion in the body reduced the mean value of minute fluctuations of body temperature and the mean spectral density of minute fluctuations in body temperature in the 2-20-min periods. This attested to a stabilizing effect of deuterium depletion on the rhythms of body temperature fluctuations, without significant shifts in the thermogenesis parameters. Thus, drinking water with reduced deuterium content makes them less sensitive to external influences.We studied the effect of various detergents (Tween-20, Triton X-100, and sodium deoxycholate) on activity and magnesium-dependent properties of Na+,K+-ATPase of the crude membrane fraction of rat cerebral cortex. All studied detergents significantly increased activity of the studied enzyme in a concentration-dependent manner. Sodium deoxycholate provided significantly higher values Na+,K+-ATPase activity (by ≈50%) than Triton X-100 and Tween-20. In the presence of Triton X-100, a changed pattern of the dependence of enzyme activity on the concentration of magnesium ions in the incubation solution was noted. Separate measurement of activities of Na+,K+-ATPase isoforms made it possible to assume that changes in magnesium-dependent properties are due to the predominant effect of Triton X-100 on ouabain-sensitive α2- and α3-isoforms.The development of morphine tolerance in C57BL/6j mice was estimated by the analgesic effect in tail-flick and hot plate tests. Morphine hydrochloride (10 mg/kg body weight) was administered to animals twice for 5 days and once on the sixth day, saline or myelopeptides were injected 15 min before morphine administration (2 μg/kg body weight). In the tail-flick test, all studied myelopeptides suppressed the development of tolerance to morphine and did not show their own analgesic activity. In the hot plate test, only three myelopeptides (MP2, MP5, and MP6) were found to reduce the formation of morphine tolerance. MP1 significantly reduced the analgesic effect of morphine on days 1-3 of administration, but contributed to the preservation of the analgesic effect during the period of tolerance development.The phenomenon of ischemic preconditioning was discovered in 1986 in experiments with the heart, and then it was observed in almost all organs, the kidneys included. This phenomenon is underlain by conditioning of the tissues with short ischemia/reperfusion cycles intended for subsequent exposure to pathological ischemia. Despite the kidneys are not viewed as so vital organs as the brain or the heart, the acute ischemic injury to kidneys is a widespread pathology responsible for the yearly death of almost 2 million patients, while the number of patients with chronic kidney disease is estimated as hundreds of millions or nearly 10% adult population the world over. Currently, it is believed that adaptation of the kidneys to ischemia by preconditioning is the most effective way to prevent the development of acute kidney injury, so deep insight into its molecular mechanisms will be a launch pad for creating the nephroprotective therapy by elevating renal tolerance to oxygen deficiency. This review focuses on the key signaling pathways of kidney ischemic preconditioning, the potential pharmacological mimetics of its key elements, and the limitations of this therapeutic avenue associated with age-related decline of ischemic tolerance of the kidneys.
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