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Biomedical subjects

A Lachowicz

Publications and source records attributed to A Lachowicz.

16 recordsLinked to original sources
PubMed2005

Nutritional status of patients hospitalised in Poland.

AIM: Screening and extended assessment of the nutritional status of patients on admission and on discharge from hospital were carried out. DESCRIPTION: The studies were carried out in four teaching hospitals, four provincial hospitals and four county hospitals in Poland. SUBJECTS: Screening examinations were carried out for 3310 randomly selected patients (every 10th patient admitted to hospital, including 1916 female cases aged from 16 to 92 y and 1394 male patients aged from 16 to 100 y). Extended examinations were carried out on 210 patients aged from 16 to 87 y (including 122 female and 88 male). MAIN ASSESSMENT PARAMETERS: Anthropometric (height, weight, body mass index (BMI), waist-to-hip ratio (WHR), arm circumference) and biochemical indices (erythrocyte count, haemoglobin concentration, white blood cell count, blood lymphocyte count and serum albumin serum concentration). The extended examinations included determination of antioxidant vitamins (A, C, E), vitamin B(12) and folic acid. RESULTS: On admission to hospital, 10.43% of the patients surveyed had a BMI below 20 kg/m(2), in 20.74% of patients serum albumin concentration was below 3.5 g/dl, indicating possible protein energy malnutrition. In addition, 21.02% had lymphocyte count below 1.5 x 10(3)/mm(3). During hospitalisation, deterioration in the nutritional status of the patient population occurred. On discharge from hospital, the percentage of patients with BMI < 20 kg/m(2) increased to 11.21% and the percentage with low blood albumin (<3.5 g/dl) increased to 28.57%. On admission, vitamin C deficiency was present in 51.8% of patients, folic acid deficiency in 32%, vitamin E deficiency in 10%, vitamin B(12) deficiency in 6.8% and vitamin A deficiency in 1.4%. Vitamin deficiencies were present equally in malnourished, overweight and obese patients. CONCLUSIONS: In patients admitted to hospitals in Poland, malnutrition risk demonstrated by BMI was observed in 10.43% of patients. On the basis of biochemical indices, increased nutritional risk was demonstrated in 21% of patients. Vitamin malnutrition was seen in the majority of patients. A significant correlation between weight, BMI, arm circumference, blood lymphocyte count and the number of days spent in hospital was observed. SPONSORSHIP: The Committee of Scientific Research and the Ministry of Health-PBZ 012-14.

Adolescent↗
PubMed2005

Estradiol modulates the synapsins phosphorylation by various protein kinases in the rat brain under in vitro and in vivo conditions.

Synapsins are the neuronal phosphoproteins which play very important role in processes of synaptic neurotransmission. They are physiological substrates for Ser/Thr protein kinases. The reversible phosphorylation of synapsins may be modified by several compounds including steroid hormones. The aim of our study was to investigate, if the one of neuroactive steroid--17beta-estradiol--could modulate the phosphorylation of synapsins by PKA, CaM-PK and PKC in rat brain and what type of mechanism of their action is possible. The activity of kinases was evaluated as phosphorylation of synapsin in cerebral cortex and hippocampus in vivo and in vitro conditions. We conclude that 17E2 has inhibitory effect on synapsins phosphorylation by all tested kinases in vitro and in vivo conditions. The lack of nuclei in synaptosomal membrane fraction and short time of hormone exposure can be evidence of direct, non-genomic mechanism of estradiol action.

Animals↗
PubMed2001

Pregnenolone sulfate modulates angiotensin II-induced inositol 1,4,5-trisphosphate changes in the anterior pituitary of female rat.

The present study was designed to test whether pregnenolone sulfate can influence the angiotensin II (AngII) action in the anterior pituitary. Female rats were ovariectomized and 10 days after operation were treated with either 50 or 250 microg per animal in one of the following substances: oil (control), pregnenolone sulfate (PREG-S), estradiol benzoate (E(2),) progesterone (P), or dehydroepiandrosterone sulfate (DHEA-S), given in single intraperitoneal injection. Because AngII is known to act in the anterior pituitary through the phosphatidiloinositol breakdown, thus increasing the level of inositol-1,4,5-trisphosphate (IP(3)), the IP(3) concentration was determined 24 h after the injection in the anterior pituitary homogenate after in vitro exposure to AngII. Among the tested steroids only PREG-S enhanced the basal (without AngII) and AngII-induced level of IP(3) in both doses used. There was no difference between the effect of a high and low dose of PREG-S. These results show that PREG-S may modulate AngII action in the anterior pituitary, regardless of the presence of ovary.

Adjuvants, Immunologic↗
PubMed2001

Corticotrophin-releasing hormone and ACTH levels in maternal and fetal blood during spontaneous and oxytocin-induced labour.

The changes in corticotrophin-releasing hormone (CRH), ACTH and dehydroepiandrosterone (DHEA) in maternal and fetal plasma were estimated in women undergoing spontaneous and oxytocin-induced labour to correlate hormone changes with the mode of parturition. Blood was sampled from a maternal peripheral vein 2 days before labour, during the second stage of labour and on the second postnatal day, and also from umbilical vessels just after delivery. Hormone concentrations were measured by RIA and ELSA methods. The maternal plasma CRH concentration before labour was significantly higher in the group of women delivered spontaneously and declined during the labour through to the second postnatal day. Measured in umbilical vessels, CRH as well as ACTH concentrations were higher in the umbilical vein than artery. The mean maternal plasma ACTH was similar in both groups before delivery, then increased significantly in both groups during the labour, decreasing on the second day after delivery. There were no changes in DHEA concentrations among the groups and at all time points of collection. No correlations between CRH and ACTH or DHEA were observed. Our results suggest that the maternal pituitary can respond to stress factors during delivery but peripheral CRH, probably mainly of placental origin, is not a major modulator of pituitary action.

Adrenocorticotropic Hormone↗
PubMed2000

Effect of 17-beta-estradiol and progesterone on angiotensin II-induced changes in inositol-1,4,5-trisphosphate content and protein kinase C activity in anterior pituitary.

Angiotensin II (AngII) is known to act in the anteriorpituitary through phosphatidiloinositol breakdown, increasing the level of inositol-1,4,5-trisphosphate (IP(3)) and diacyloglycerol (DAG), a potential activator of protein kinase C (PKC). We examined the effect of estradiol and progesterone treatment in vivo on IP(3) levels and activity of PKC under the influence of AngII. Three groups of intact female rats received in vivo injections of 17-beta-estradiol, progesterone, and oil (control) for five days, and then the in vitro effect of AngII was examined using homogenate of the anterior pituitary. AngII increased either the IP(3) concentration or the synapsin I phosphorylation catalyzed by PKC. Estradiol enhanced the basal (without AngII) IP(3) level and PKC activity induced by AngII. Progesterone did not change the basal and AngII-induced IP(3) concentrations. On the other hand, it decreased the basal PKC activity and blocked the effect of AngII. Our data suggest that ovarian steroids can modulate the effect of AngII on the anterior pituitary gland.

Angiotensin II↗
PubMed1997

Uncoupling of calcium mobilization and entry pathways in endothelin-stimulated pituitary lactotrophs.

In cells expressing Ca2+-mobilizing receptors, InsP3-induced Ca2+ release from intracellular stores is commonly associated with extracellular Ca2+ influx. Operation of these two Ca2+ signaling pathways mediates thyrotropin-releasing hormone (TRH) and angiotensin II (AII)-induced prolactin secretion from rat pituitary lactotrophs. After an initial hyperpolarization induced by Ca2+ mobilization from the endoplasmic reticulum (ER), these agonists generated an increase in the steady-state firing of action potentials, further facilitating extracellular Ca2+ influx and prolactin release. Like TRH and AII, endothelin-1 (ET-1) also induced a rapid release of Ca2+ from the ER and a concomitant spike prolactin secretion during the first 3-5 min of stimulation. However, unlike TRH and AII actions, Ca2+ mobilization was not coupled to Ca2+ influx during sustained ET-1 stimulation, as ET-1 induced a long-lasting abolition of action potential firing. This lead to a depletion of the ER Ca2+ pool, a prolonged decrease in [Ca2+]i, and sustained inhibition of prolactin release. ET-1-induced inhibition and TRH/AII-induced stimulation of Ca2+ influx and hormone secretion were reduced in the presence of the L-type Ca2+ channel blocker, nifedipine. Basal [Ca2+]i and prolactin release were also reduced in the presence of nifedipine. Furthermore, TRH-induced Ca2+ influx and secretion were abolished by ET-1, as TRH was unable to reactivate Ca2+ influx and prolactin release in ET-1-stimulated cells. Depolarization of the cells during sustained inhibitory action of ET-1, however, increased [Ca2+]i and prolactin release. These results indicate that L-type Ca2+ channel represents a common Ca2+ influx pathway that controls basal [Ca2+]i and secretion and is regulated by TRH/AII and ET-1 in an opposite manner. Thus, the receptor-mediated uncoupling of Ca2+ entry from Ca2+ mobilization provides an effective control mechanism in terminating the stimulatory action of ET-1. Moreover, it makes electrically active lactotrophs quiescent and unresponsive to other calcium-mobilizing agonists.

Action Potentials↗
PubMed1995

Estradiol and pregnenolone sulfate could modulate PMA-stimulated and Ca2+/calmodulin-dependent synaptosomal membrane protein phosphorylation from rat brain in vivo.

We have examined the effect of two steroids, pregnenolone sulfate and 17-beta-estradiol, on the activity of two protein kinases: protein kinase C and Ca2+/calmodulin-dependent protein kinase. The activity of the kinases was evaluated as phosphorylation of two synapsins Ia and Ib in cerebral cortex and hippocampus of the rat brain. Both steroids decreased phosphorylation of both synapsins to a great extent; however, in hippocampus neither pregnenolone nor estradiol influenced the reaction catalyzed by Ca2+/calmodulin-protein kinase. In the remaining areas of the brain estradiol decreased the activity of both studied kinases to a greater degree than pregnenolone sulfate. Our study suggests that pregnenolone sulfate and 17-beta-estradiol could modulate directly Ca2+/calmodulin-dependent protein kinase and protein kinase C and thus directly influence processes of neurotransmission.

Animals↗
PubMed1994

Somatostatin-14 increases the inositol-1,4,5-trisphosphate content in various areas of the brain.

The effects of somatostatin-14 on inositol-1,4,5-trisphosphate (IP3) content were examined in rat pituitary, hippocampus and cortex homogenates. Somatostatin increased IP3 concentration in all these investigated regions in a dose- and time-dependent manner. Maximal increase of IP3 content was found in the pituitary homogenate, and in the hippocampal and cortex homogenates the IP3 argumentation was slightly smaller. Time-response studies showed that this effect declined with extended time of incubation. These results suggest that IP3 is involved in the mechanism of action of somatostatin in brain.

Analysis of Variance↗
PubMed1993

Failure of tripeptide colon mitosis inhibitor to suppress the cell proliferation of dimethylhydrazine-induced colonic cancers in rats.

The effects of tripeptide colon mitosis inhibitor (CMI, pGlu-His-Gly-OH) on the proliferation of tumoral cells of dimethylhydrazine (DMH)-induced colonic cancers in rats were studied. Additionally, the effects of CMI on hyperplastic colonic crypts in DMH-treated rats and on normal colonic crypts in carcinogen-untreated rats were estimated. As an index of the cell proliferation the incorporation of bromodeoxyuridine (BrDU) into cell nuclei was used. It was found that the tripeptide significantly suppressed the proliferation of the colonic crypts in normal, carcinogen-untreated rats. However, it failed to suppress the cell proliferation of DMH-induced colonic adenocarcinomas or adenomas and produced only a slight, statistically insignificant decrease of the BrDU labelling index in hyperplastic colonic mucosa of DMH-treated rats. These findings suggest that the process of carcinogenesis might 'switch off' the local negative control of the colonic cell proliferation exerted by endogenous CMI.

Adenocarcinoma↗
PubMed1993

Comparison of the antiproliferative effects of colon mitosis inhibitor, thyroliberin and the somatostatin analog octreotide on rat colonic mucosal epithelial cells.

The effects of colon mitosis inhibitor (CMI), thyroliberin (TRH), and the somatostatin analogue octreotide (SMS 201-995) on rat colonic mucosal epithelial cell proliferation were studied. As an index of cell proliferation the incorporation of bromodeoxyuridine (BrDU) into cell nuclei was used. It was found that all three peptides inhibited the colonic mucosal epithelial cells proliferation, but the time course of inhibition was different. The effect of SMS 201-995 occurred 12 h after the peptide injection, while CMI and TRH suppressed the proliferation after 24 h. These observations suggest that the mechanisms of the antiproliferative actions of somatostatin and of related tripeptides CMI and TRH are different.

Animals↗
PubMed1992

Effects of somatostatin on inositol-1,4,5-trisphosphate content in mouse spleen lymphocytes.

1. The effects of somatostatin-14 (SS) and diazepam in vitro on the content of inositol-1,4,5-trisphosphate (IP3) in mouse spleen lymphocytes were investigated. 2. It was found that the exposure of mouse spleen lymphocytes in vitro to SS sharply diminished their IP3 level. 3. Diazepam had no effect on lymphocytes IP3 content. 4. The inhibition of phosphatydyloinositol (PI) breakdown was suggested as one of the mechanisms of the physiological SS action.

Animals↗
PubMed1991

Effects of somatostatin-14 and its analogs on the (Ca,Mg)ATPase in the rat anterior pituitary.

The effects of somatostatin-14 and its biologically active analogs, RC-160 and SMS 201-995, on (Ca,Mg)ATPase activity in vitro were studied in homogenates of anterior pituitary cells. It was found that somatostatin inhibited the (Ca,Mg)ATPase activity in the anterior pituitary and somatostatin analogs exerted slight biphasic effects on the calcium pump activity. The effects of specific brain (Ca,Mg)ATPase inhibitors, VOSO4 and LaCl3, were also studied in vitro. Neither VOSO4 nor LaCl3 enhance the inhibition of calcium pump activity caused by somatostatin. It is suggested that somatostatin may mediate its action in pituitary cells, among others, by the regulation of (Ca,Mg)ATPase activity.

Animals↗
PubMedDate not supplied

Angiotensin II changes inositol-1,4,5-trisphosphate content in the pituitary and hypothalamus but not in cerebral cortex of the rat brain.

The present study was undertaken to investigate the effect of angiotensin II (AngII) on the concentration of inositol-1,4,5-trisphosphate (IP3) and the modulation of AngII action by estradiol in the brain. Our studies were conducted in male rat anterior pituiary, hypothalamus and cerebral cortex with and without previous estradiol treatment. In the cerebral cortex, there were no changes in IP3 content after exposure to AngII. In the anterior pituitary, AngII increased the IP3 concentration at all doses studied. However, in the hypothalamus, AngII decreased the IP3 concentration and its effect was also time dependent. Prior treatment with estradiol intensified the effects of AngII action on IP3 concentrations, in both the pituitary (increase) and hypothalamus (decrease). These results indicate that in the male rat anterior pituitary, AngII increases phosphatidiloinositol hydrolysis, leading to the increased production of the intracellular messenger, IP3. The decrease of IP3 concentration observed in the hypothalamus suggests a different site of AngII action in this region. We also suggest that estrogens can modulate AngII action in the brain.

Analysis of Variance↗