Assessment and prevalence of depression in women 45-55 years of age visiting gynecological clinics in Poland: screening for depression among midlife gynecologic patients.

The aims of the Polish survey were to assess efficacy of screening for depression in gynecological practice and to estimate prevalence of depressive disorders in midlife women visiting gynecologists. The study included 2262 female outpatients aged 45-55, who were screened by 120 gynecologists throughout Poland. Patients completed the Beck's Depression Inventory (BDI) and were assessed by gynecologists to verify the presence of symptoms of a current Depressive Episode according to ICD-10 diagnostic criteria. Patients who obtained a score of 12 points or more on the BDI were referred for psychiatric evaluation, including the modified version of Mini International Neuropsychiatric Interview (MINI). The study showed that gynecologists in Poland are able to perform screenings for depression effectively in outpatient settings. Results also suggested that about 19% of women aged 45 to 55 years visiting gynecologists may suffer from depressive disorders.

Ultrafiltration of Micellar Solutions Containing Phenols.

Micellar-enhanced ultrafiltration represents a potentially attractive tool for the removal of different contaminants from wastewaters. The ultrafiltration of micellar solutions containing phenol or 4-nitrophenol was studied. Sodium dodecyl sulfate (SDS), hexadecyltrimethyl ammonium sulfate, alkyl polyglucoside Glucopon 215 SC UP, and oxyethylated methyl dodecanoates with the average degree of oxyethylation equal to 5 and 9 were used as surfactants and NaHCO(3) as an electrolyte and alkalizing agent. Filtration and phenol rejection depends on the presence of NaHCO(3) and the type of surfactant. NaHCO(3) depresses to the filtration rate, especially in the case of SDS and hydrophobic oxyethylated methyl dodecanoate. The highest filtration rates are obtained for hexadecyltrimethyl ammonium bromide (CTAB) and alkyl polyglucoside micellar solutions. The best separations, both of phenol and 4-nitrophenol (almost 100% rejection), are obtained for CTAB micellar solutions at the pH range from 3 to 11. Nonionic surfactants are not effective enough for the separation of phenol and 4-nitrophenol. SDS solutions permit only the separation of phenol. Copyright 1999 Academic Press.

Creatine supplementation differentially affects maximal isometric strength and time to fatigue in large and small muscle groups.

Ten physically active, untrained, college-aged males (26.4 +/- 5. 8 years old) received creatine (CR, 5 g creatine monohydrate + 3 g dextrose) and placebo (PLA, 7 g dextrose) supplementation four times per day for 5 days in a double-blind, randomized, balanced, crossover design. Performance was assessed during maximal and three repeated submaximal bouts of isometric knee extension and handgrip exercise. CR supplementation significantly increased (p <.05) maximal isometric strength during knee extension but not during handgrip exercise. CR supplementation increased time to fatigue during each of the three bouts of submaximal knee extension and handgrip exercise when compared to the PLA trials. These findings suggest that CR supplementation can increase maximal strength and time to fatigue during isometric exercise. However, the improvements in maximal isometric strength following CR supplementation appear to be restricted to movements performed with a large muscle mass.

Escherichia coli heat-stable enterotoxin receptors. A novel marker for colorectal tumors.

PURPOSE: Receptors for Escherichia coli heat-stable toxin (ST) are selectively expressed in membranes of intestinal mucosa cells and colon carcinoma cells in vitro, suggesting their use as a marker for colorectal tumors in vivo. The present studies examined the expression and function of ST receptors in normal human tissues and primary and metastatic colorectal tumors obtained from patients at surgery. METHODS: Surgical specimens were obtained as follows: from normal colon; from primary adenocarcinomas from all anatomic divisions of the colon and rectum; from gallbladder, kidney, liver, lung, lymph node, ovary, peritoneum, stomach; and from colon carcinomas metastatic to liver, lung, lymph node, ovary, and peritoneum. Membranes prepared from these specimens were assessed for the presence and functional characteristics of ST receptors. RESULTS: ST bound specifically to membranes from each division of normal colon and rectum and all primary and metastatic colorectal tumors examined. The affinity and density of ST receptors were similar in tumors of different grades and from various metastatic sites. ST-receptor interaction was coupled to activation of guanylyl cyclase in all normal samples of colon and rectum and all primary and metastatic colorectal tumors examined. In contrast, neither ST binding nor ST activation of guanylyl cyclase was detected in any extraintestinal tissues examined. CONCLUSIONS: Functional ST receptors are expressed in normal colonic tissue and primary and metastatic colorectal tumors but not by extraintestinal tissues in humans. Expression of ST receptors does not vary as a function of the metastatic site or grade of these tumors. Receptors expressed by colorectal tumors retain their characteristic function, with binding of ST coupled to activation of guanylyl cyclase. These studies support the suggestion that ST receptors represent a specific marker for human colorectal tumors that may have use as a target for directing diagnostics and therapeutics to these tumors in vivo.

Internalization of E. coli ST mediated by guanylyl cyclase C in T84 human colon carcinoma cells.

Internalization of Escherichia coli heat-stable enterotoxin (ST) mediated by guanylyl cyclase C was examined in T84 human colon carcinoma cells. Surface-associated, receptor-bound ST was quantitatively separated from intracellular ligand employing acidic guanidine-HCl. ST was internalized in a time-, temperature-, and ligand concentration-dependent fashion only by cells specifically expressing guanylyl cyclase C. Only receptors which bound reversibly to ST appeared to mediate endocytosis. The rate of internalization of ST empirically determined in these studies was 0.23 min-1. The density of surface receptors for ST was similar at 4 degrees C and 37 degrees C, suggesting that these receptors recycle back to the cell surface following internalization of ligand. Similarly, internalized ST was rapidly cleared from the intracellular compartment following endocytosis. These studies demonstrate that ST undergoes ligand-dependent receptor-mediated endocytosis in human colon carcinoma cells.

An evaluation of cocaine-induced chest pain.

STUDY OBJECTIVE: To determine if enzymatic evidence of acute myocardial injury is present in patients complaining of chest pain after cocaine use when the ECG is normal or nondiagnostic. DESIGN: Serial ECG and creatinine kinase (CK) and CK isoenzymes (CK-ISO) determinations were performed at time of emergency department presentation and every six hours over 12 hours on individuals complaining of chest pain within six hours of last cocaine use. SETTING: ED of an urban tertiary care center. TYPE OF PARTICIPANTS: Forty-two individuals with a mean age of 28.5 years. INTERVENTIONS: Patients with positive CK-ISOs were admitted immediately to formally rule out myocardial infarction. Patients developing ECG changes during observation period also were admitted even if CK-ISOs were normal. Patients with unchanged ECGs and normal CK-ISOs were discharged after 12 hours of observation. RESULTS: Eight patients (19%) had elevated CK and CK-ISO values at presentation. Two of these patients had elevated values on three sequential determinations and were believed to have sustained acute myocardial infarction. Six patients had elevated CK and CK-ISOs at presentation only. ECGs remained normal or nondiagnostic in all patients. CONCLUSIONS: Enzymatic evidence of acute myocardial injury may occur in patients who develop chest pain after cocaine use and have normal or nondiagnostic ECGs. This injury may reflect acute infarction or transient ischemia. Single or serial normal or nondiagnostic ECGs do not rule out ischemia or injury in this group of patients.

Cardiovascular effects of substance P receptor stimulation in the ventrolateral medullary pressor and depressor areas.

The pressor (VLPA) and the depressor (VLDA) areas in the ventrolateral medulla were identified with the microinjection of L-glutamate (1.77 nmol/site) in artificially ventilated urethane-anesthetized male Wistar rats. Bilateral microinjection of a stable substance P (SP) agonist [pGlu5, MePhe8, Sar9]-SP(5-11)], abbreviated as DiMe, into the VLPA (6-600 pmol/site) produced a dose-dependent increase in blood pressure (BP). The effects on heart rate (HR) were variable. Intravenous pretreatment with a ganglionic blocker chlorisondamine (3.0 mg/kg, i.v.), but not with a vasopressin antagonist, blocked these responses. Similar microinjection of DiMe (6-600 pmol/site) into the VLDA produced a dose-dependent decrease in HR but had no effect on BP levels. The DiMe-induced bradycardic response elicited from the VLDA was blocked by i.v. pretreatment with atropine methylbromide (0.5 mg/kg, i.v.). These findings indicate that there are SP receptors localized on sympathoexcitatory neurons in the VLPA and that SP may be an excitatory neurotransmitter in this area. In the VLDA, the SP receptors appear to be localized on a subpopulation of neurons that affect vagal, but not sympathetic, outflow to the heart.

Putative neurotransmitters involved in medullary cardiovascular regulation.

Experiments were carried out in artificially ventilated pentobarbital-anesthetized male Wistar rats. Following microinjection of muscimol (GABA-mimetic) or kynurenic acid (KYN; glutamate antagonist) into the ventrolateral medullary depressor area (VLDA), microinjection of L-glutamate (GLU; 4.5 nmol) into the NTS elicited a pressor response. This pressor response was attenuated in a dose-dependent manner by microinjection of KYN (0.5-5 nmol) into the ventrolateral medullary pressor area (VLPA). A GLU-induced pressor response could also be elicited from the NTS when GABA receptors in the VLPA were blocked with the microinjection of bicuculline (GABA antagonist, 200 pmol) into this site. The same dose of bicuculline in the VLPA also blocked the depressor responses elicited from the VLDA. With the VLDA or VLPA functionally unimpaired, microinjection of GLU (4.5 nmol) into the NTS elicited a fall in blood pressure and heart rate. This depressor response was attenuated in a dose-dependent manner by the microinjections of KYN (2-20 nmol) into the VLDA. These results indicate that: (1) The NTS sends glutamatergic inputs to both the VLDA and the VLPA; the projection from the NTS to the VLPA mediates pressor responses while that from the NTS to the VLDA represents one component of the pathway mediating the depressor responses elicited from the NTS. (2) The pathway from the VLDA to the VLPA is GABA-ergic and represents another component of the pathway mediating depressor responses evoked from the NTS. (3) The bradycardia evoked from the NTS may involve a pathway from the NTS to the VLDA.

Evidence for a sympathoexcitatory pathway from the nucleus tractus solitarii to the ventrolateral medullary pressor area.

The role of the ventrolateral medullary pressor (VLPA) and depressor (VLDA) areas in mediating cardiovascular responses evoked from the nucleus tractus solitarius (NTS) was investigated. Male Wistar rats, anesthetized with pentobarbital or urethane, were artificially ventilated and blood pressure (BP) and heart rate (HR) were monitored. The VLPA, VLDA, and the NTS were identified bilaterally with microinjections of L-glutamate. Unilateral microinjections of muscimol or lidocaine into the VLPA or the VLDA blocked the decrease in BP produced by microinjections of L-glutamate (1.77 nmol) into the NTS. These findings indicate that both areas are essential for mediating depressor responses elicited from the NTS. When neuronal activity in the VLDA was depressed unilaterally (leaving the ipsilateral VLPA intact), with the microinjection of muscimol or lidocaine, microinjection of a larger dose (5.0 nmol) of L-glutamate into the ipsilateral NTS elicited a pressor response. This response was blocked by depressing neuronal activity in the ipsilateral VLPA by microinjection of muscimol into this site. This pressor response evoked from the NTS was not due to non-specific effects of L-glutamate since repeated microinjections of L-glutamate (5.0 nmol/site) into the NTS consistently produced decreases in BP and HR. The stimulation of the contralateral NTS by glutamate continued to elicit the usual decreases in BP and HR. Microinjections of either dose (1.77 or 5 nmol) of L-glutamate into the areas adjacent to the NTS (e.g. 1.0 mm rostral or lateral to the NTS, the gracile or cuneate nuclei and area postrema) failed to evoke any cardiovascular responses indicating that the responses were mediated by neurons localized within the intermediate one-third of the NTS. These results indicate that: (1) the depressor responses elicited from the NTS involve the pathways from the NTS to the VLDA and VLDA to VLPA and (2) there may be a pathway from the NTS to the VLPA which is sympathoexcitatory and is unmasked when neuronal activity in the VLDA is depressed.

Ventrolateral medullary pressor area: site of hypotensive action of clonidine.

Intravenous injections of clonidine produce an initial transient increase in blood pressure followed by a long-lasting hypotension and bradycardia. The initial pressor response is due to activation of vascular alpha 1-adrenergic receptors while the hypotension and bradycardia are caused by the central actions of clonidine. Although, hypothalamus, nucleus tractus solitarius (NTS), ventrolateral medulla and the intermediolateral cell column of the thoracolumbar spinal cord (IML) have been implicated, the exact site of these actions of clonidine in the central nervous system is not established. The results of this investigation suggest that the pressor area in the ventrolateral medulla (VLPA) is the site of hypotensive and bradycardic actions of intravenously administered clonidine. This conclusion is based on the observation that microinjections of idazoxan, a specific alpha 2-adrenergic receptor blocker, into the VLPA prevented and reversed the hypotension and bradycardia despite the fact that other proposed sites of these actions (NTS, hypothalamus and IML) were intact and accessible to intravenously administered clonidine.

Examination of the filterability of oxygenated erythrocytes (containing normal, trait or sickle cell disease type hemoglobins) in the presence of L-epinephrine, D,L-isoproterenol or prostaglandins (PG) A1, A2, E1, E2, F1alpha or F2alpha.

These studies were directed toward determining effects of selected vasoactive compounds on oxygenated erythrocytes. Considering the major circulatory effects that small changes in blood flow might initiate in sickle cell anemia patients, erythrocytes from individuals with this disease and from one person with the trait condition were included. PGA1, PGE1, and PGE2 significantly increase filtration times in normal erythrocytes (AA-type hemoglobin) at 10(-11) M by this method. From studies of the effects of L-epinephrine, D,L-isoproterenol, PGA1, PGA2, PGE1, PGE2, PGF1alpha and PGF2alpha on red blood cell filterabilities, the following observations and conclusions appear to hold: (1) Erythrocytes from different individuals (or from the same individual at different times) vary greatly in responses to these compounds. Effects of vasoactive compounds upon red cell filterability may be positive, negligible or negative. Decreased filterability (positive effect) was seen more frequently than increased. (2) Effects are observed with all compounds on some erythrocyte preparation at every concentration tested (10(-5), 10(-7), 10(-9), 10(-11) M). (3) Where epinephrine showed significant positive effect, PGA2 and PGE2 did also when tested. The reverse was not always true. (4) For PGA and PGE analogs, the subscript 2 analogs affected filterability more frequently. (5) When significant average effects for a group of donors were produced by a given compound at a particular concentration, these effects were positive for the donors studied.