Biomedical subjects

K Decker

Publications and source records attributed to K Decker.

At least 37 records · Page 2Linked to original sources

PubMed1996

How many general surgeons do you need in rural areas? Three approaches to physician resource planning in southern Manitoba.

OBJECTIVE: To assess critically the results of using three different approaches to planning for the number of general surgeons in rural areas. DESIGN: Estimates of the number of general surgeons needed using a ratio approach, a and a population-needs-based approach. SETTING: Rural southern Manitoba. OUTCOME MEASURE: Number of general surgeons needed. RESULTS: The ratio approach supported the recruitment of 7.8 to 14.5 additional general surgeons to rural southern Manitoba. The repatriation approach suggested that the area might support five additional general surgeons, if residents could be persuaded to undergo their surgery closer to home. The population-needs-based approach suggested that the health status of area residents was similar to that of residents of other areas of the province and that they had a higher rate of surgery than residents of other areas; no additional surgeons were apparently needed. CONCLUSIONS: Each method has certain advantages, and none is necessarily useful in isolation. Hence, the most effective approach to planning for general surgeons is likely a combination of all three methods. Other factors that may be important include the type of payment structure and the need for professional groups to monitor variations in rates of surgery.

Aged↗

PubMed1996

Is there a direct retina-raphe-suprachiasmatic nucleus pathway in the rat?

Possible pathways from the retina to the suprachiasmatic nucleus (SCN) relaying in the dorsal raphe nucleus (DRN) were investigated in rats using combined anterograde and retrograde tracing with immunohistochemistry. After injection of wheat germ agglutinin-conjugated horseradish peroxidase-colloidal gold complex into the SCN, many neurons were retrogradely labeled in the middle levels of the DRN. Approximately one half of these neurons contained serotonin. After injection of cholera toxin B subunit into the eyes, a few anterogradely labeled afferent fibers were detected in the rostral DRN, however, not in contact with retrogradely labeled neurons. Our findings provide direct evidence that serotonergic projections to the rat SCN stem from the DRN nuclei. They also suggest that retina-raphe-SCN projections, a presumed third visual input to the mammalian circadian pacemaker, may include further neuronal connections or brain sites.

Animals↗

PubMed1996

Hormonal, syndromal and EEG mapping studies in menopausal syndrome patients with and without depression as compared with controls.

UNLABELLED: The aim of the study was to investigate brain function in menopausal depression by EEG mapping, as compared with menopausal syndrome patients without depression and normal controls, and to correlate neurophysiological with clinical and hormonal findings in order to elucidate the pathogenesis of depression in the menopause. METHODS: One hundred and twenty-nine menopausal women, aged 45-60 years, with no previous hormonal replacement therapy were investigated in regard to hormones (estradiol [E2], follicle stimulating hormone [FSH]), clinical symptomatology (Kupperman Index [KI], Hamilton depression score [HAMD]) and brain function (EEG mapping). Based on KI and DSM-III-R research criteria for major depression, 3 groups were available for statistics (after removal of protocol violators): group A had a KI of <15 and no depression (n = 29); group B had a KI of > or = 15 and no depression (n = 29) and group C had a KI of > or = 15 and fulfilled the criteria for major depression (n = 60). RESULTS: EEG maps of depressed patients demonstrated less total power and absolute power in the delta, theta and beta band, more relative delta and less alpha power as well as a slower delta/theta and faster alpha and beta centroid than controls, suggesting a vigilance decrement. Group B did not differ from group A. Correlation maps showed significant relationships between estradiol levels and EEG measures (the lower the E2, the worse the vigilance) and between the EEG measures and the Hamilton depression (HAMD) score (the worse the vigilance, the higher the depression score). There were no correlations between the hormones E2 and FSH and the syndromes KI and HAMD. In the target variable, the asymmetry index, depressed patients showed less alpha power over the right than left frontal lobe, whereas normal controls exhibited the opposite. Group B did not differ from group A. The frontal asymmetry index was significantly correlated with the Hamilton depression score and suggests right frontal hyper- and left frontal hypoactivation in depression. CONCLUSIONS: Although hormonal findings are not directly linked to psychic changes, low estradiol levels do contribute to a decreased vigilance at the neurophysiological level , which is in turn correlated with higher depressive and menopausal symptomatology at the behavioural level. Depression is further correlated to a right frontal hyper- and left frontal hypoactivation.

Brain↗

PubMed1995

Hyperosmolarity stimulates prostaglandin synthesis and cyclooxygenase-2 expression in activated rat liver macrophages.

The effect of aniso-osmotic exposure on the level of inducible cyclooxygenase (Cox-2) and on prostanoid synthesis was studied in cultured rat liver macrophages (Kupffer cells). In lipopolysaccharide (LPS)- or phorbol 12-myristate 13-acetate-stimulated Kupffer cells, hyperosmotic (355 mosmol/l) exposure, due to addition of NaCl or impermeant sugars, markedly increased prostaglandin (PG) E2, D2 and thromboxane B2 synthesis in a time- and osmolarity-dependent manner. Increased prostanoid production was observed about 8 h after exposure to LPS in hyperosmotic medium compared to Kupffer cells treated with LPS under normotonic (305 mosmol/l) conditions. A similar stimulatory effect of hyperosmolarity on PGE2 production was also seen when arachidonate was added exogenously. Hyperosmotic stimulation of PGE2 production was accompanied by a strong induction of Cox-2 mRNA levels and an increase in immunoreactive Cox-2, whereas the levels of immunoreactive phospholipase A2 and cyclooxygenase-1 did not change significantly. Dexamethasone, indomethacin and the selective Cox-2 inhibitor, NS-398, abolished the hypertonicity-induced stimulation of PGE2 formation; dexamethasone also prevented the increase in Cox-2 mRNA and protein. The increase of immunoreactive Cox-2 lasted for about 24 h and was also blocked by actinomycin D or cycloheximide, but not by brefeldin A. Tunicamycin or treatment with endoglucosidase H reduced the molecular mass of hypertonicity-induced Cox-2 by 5 kDa. Tunicamycin treatment also suppressed the hypertonicity-induced stimulation of PGE2 production. The hyperosmolarity/LPS-induced stimulation of prostaglandin formation was partly sensitive to protein kinase C inhibition but was not accompanied by an increase in the cytosolic free Ca2+ concentration. The data suggest that osmolarity may be a critical factor in the regulation of Cox-2 expression and prostanoid production in activated rat liver macrophages.

Adenosine Triphosphate↗

PubMed1995

Nitric oxide synthase in the hypothalamic suprachiasmatic nucleus of rat: evidence from histochemistry, immunohistochemistry and western blot; and colocalization with VIP.

Nitric oxide (NO) is a neuroactive substance of high potency. Physiological results revealed the involvement of NO in circadian regulation of rats. Since neuronal structures containing NO-synthase (NOS) were previously not found in the circadian oscillator, the hypothalamic suprachiasmatic nucleus (SCN), in this species but are present in the hamster, we investigated the distribution of NO-producing structures in the rat SCN by Western blot analysis, immunohistochemistry of NOS, and by histochemistry (NADPH-diaphorase (NADPH-d) activity of NOS). Western blot analysis of SCN homogenates from rat (and, for comparison, hamster) showed a NOS-like immunoreactive (-LI) protein band of apparent molecular mass of 150 kDa, consistent with the neuronal NOS molecule. In the rat SCN, perikarya exhibiting NADPH-d staining of NOS-LI with a complete overlapping of both were found. Double-immunofluorescence experiments revealed that NOS cells are a subgroup of the neuronal SCN population that is characterized by immunoreactivity to vasoactive intestinal polypeptide. These data provide evidence for the existence of neuronal nitric oxide synthase in the rat SCN and may explain the involvement of NO in the mediation of photic information.

Animals↗

PubMed1995

Differential activation of transcription factors NF-kappa B and AP-1 in rat liver macrophages.

Liver macrophages (Kupffer cells) respond to many stimulations with the production of bioactive substances including cytokines, eicosanoids, and inorganic radicals. In this study the activation of transcription factors by substances inducing cytokine gene expression or superoxide formation in rat Kupffer cells was examined. Using primary cultures of rat Kupffer cells the role of NF-kappa B and activator protein 1 (AP-1) in the expression of the tumor necrosis factor-alpha (TNF-alpha) gene by lipopolysaccharide (LPS) was investigated. Both transcription factors were strongly activated but with different kinetics. Maximal DNA-binding activity was induced with 50 ng of LPS/mL of medium and persisted for at least 24 hours. At that time, NF-kappa B- as well as AP-1-DNA complexes decreased their mobilities in native gels. Among the cytokines tested only TNF-alpha and macrophage colony-stimulating factor (M-CSF) were able to activate NF-kappa B in Kupffer cells. Phorbol ester and zymosan activated AP-1 but not NF-kappa B; the treatment of zymosan yielding a modified form of AP-1. Of all substances found to interfere with TNF-alpha production by Kupffer cells (pyrrolidine dithiocarbamate, dexamethasone, prostaglandin E2, interleukin [IL]-4, IL-10, and transforming growth factor-beta [TGF-beta]) only pyrrolidine dithiocarbamate was able to completely inhibit the activation of NF-kappa B by LPS. Although not abrogating the LPS activation of NF-kappa B, dexamethasone inhibited that of AP-1. The results indicate a direct participation of NF-kappa B in the regulation of TNF-alpha synthesis and a differential effect of LPS on NF-kappa B and AP-1, respectively.

Animals↗

PubMed1995

Demonstration of retinal afferents in the RCS rat, with reference to the retinohypothalamic projection and suprachiasmatic nucleus.

In the Royal College of Surgeons (RCS) rat, characterized by inherited retinal dystrophy, retinal projections to the brain were studied using anterograde neuronal transport of cholera toxin B subunit upon injection into one eye. The respective immunoreactivity was found predominantly contralateral to the injection site in the lateral geniculate nucleus, superior colliculus, nucleus of the optic tract, medial terminal nucleus of the accessory optic tract, and bilateral hypothalamic suprachiasmatic nuclei. Although terminal density was somewhat reduced in dystrophic rats, the projection patterns in these animals appeared similar to those seen in their congenic controls and were comparable to the visual pathways described for the rat previously. In dystrophic rats, the number of cell bodies exhibiting immunoreactivity to vasoactive intestinal polypeptide, viz. a population of suprachiasmatic neurons receiving major retinohypothalamic input, was reduced by one-third, and some differences were observed in the termination pattern of the geniculohypothalamic tract, as revealed by immunoreactivity to neuropeptide Y in the suprachiasmatic nucleus.

Afferent Pathways↗

PubMed1995

Action of endothelins on hepatic stellate cells.

To elucidate the role played by hepatic sinusoidal cells in the regulation of the circulatory status in the liver, the effect of endothelins (ETs) on primary-cultured stellate cells was examined. Kinetic analysis with 125I-labeled ET-1 revealed that stellate cells have ET receptors with a Kd value of 141 pM and a Bmax of 12.3 fmol/10(5) cells. ET-1, -2, and -3 dose-dependently increased inositol monophosphate (InsP) levels in stellate cells with an EC50 of 0.53, 1.63, and 1.88nM, respectively. Binding of 125I-labeled ET-1 to stellate cells and the ET-enhanced InsP formation were suppressed by preincubating the cells with 10 nM of unlabeled ET-1 or ET-3 for more than 3 h, indicating down-regulation and desensitization of ET receptors by homologous ligands. Binding of ETs to surface receptors induced a marked contraction of stellate cells. Stellate cells rapidly reacted to ETs, as detected by the flexible silicone-rubber-membrane method; 78%, 73%, and 58% of the stellate cells contracted 2.5 min after the addition of 10 nM of ET-1, ET-2, or ET-3, respectively. On the other hand, ETs also triggered a long-lasting contraction of the cells, as revealed with hydrated collagen gels. The ET-induced contraction of stellate cells decreased the diameter of the collagen lattice by about 60%, and this action was inhibited either by cytochalasin B or by H-7, a protein kinase C inhibitor. These and other results suggest that ETs induced cell contraction by some mechanism that involved protein kinase C.

Animals↗

PubMed1995

A psychiatrist-rated battery of measures for assessing the clinical status of psychiatric inpatients.

Despite the increasing demand for outcome assessment measures, no published reports have provided a standardized way to assess psychiatric inpatients that includes diagnosis and observer ratings of psychopathology. This paper reviews general principles for selecting outcome assessment measures, proposes a battery of instruments based on already available measures to assess clinical status in psychiatric inpatients, reviews methods of implementing the battery in an academic inpatient psychiatric setting, and presents preliminary data on its interrater reliability, construct validity, and range of response to acute hospitalization. Preliminary results suggest that the battery may be useful for resident and medical student education and for enhancing quality assurance and continuous quality improvement.

Comorbidity↗

PubMed1994

Nitric oxide-synthesizing neurons in the hamster suprachiasmatic nucleus: a combined NOS- and NADPH- staining and retinohypothalamic tract tracing study.

Neuronal nitric oxide (NO), thought to be a neuroactive substance of high potency, is produced by the enzyme nitric oxide synthase (NOS) which has been demonstrated to additionally exhibit a so-called NADPH-diaphorase (NADPH-d) activity. Since physiological results pointed to the involvement of NO in circadian regulation, and morphological descriptions are not available, we sought to study the distribution of NO-producing cells in the hypothalamic suprachiasmatic nucleus (SCN) in Djungarian hamsters (Phodopus sungorus) by means of histochemistry and immunohistochemistry (IHC). In the SCN, NADPH-d stained perikarya of varying intensity and number were found predominantly in the ventrolateral subdivision. Diaphorase staining combined with the IHC demonstration of NOS revealed a complete overlapping of both. The combination of NADPH-d staining with the demonstration of the retinohypothalamic tract using the anterograde neuronal transport of cholera toxin B (CTB) following intraocular injection showed CTB terminals accumulating at NADPH-d cell bodies mainly in the ventrolateral region of the SCN. These data provide morphological evidence for the involvement of nitric oxide in the mediation of photic stimulation of the circadian oscillator located in the SCN.

Animals↗

PubMed1994

Nitric oxide production by cells isolated from regenerating rat liver.

Nitric oxide (NO) production by cells of the regenerating liver was estimated from the amount of nitrite accumulated during 24 h in the culture media of hepatocytes, Kupffer cells and sinusoidal endothelial cells isolated at different times after partial hepatectomy (PHE). The time course of NO production was compared with the course of the proliferating activity of the same cells. During the time when liver cells pass through their first cell cycles, hepatocytes were the main producers of NO in the liver. The time-dependent changes of their NO production corresponded to those obtained with the whole liver and were inversely correlated with the DNA-synthesizing activity. The NO production by Kupffer and endothelial cells followed that by hepatocytes in this order; the time displacement between them corresponded to the schedule of their proliferating activity. The NO synthesis in non-parenchymal cells fluctuated in a similar way as in parenchymal cells and was minimal when DNA synthesis was manifest.

Animals↗

PubMed1994

Epr evidence of nitric oxide production by the regenerating rat liver.

Nitric oxide (NO) production in the regenerating liver was estimated from the intensity of the electron paramagnetic resonance (e.p.r.) signal of the mononitrosyl complexes of iron and diethylthiocarbamate (DETC). Preformed complexes of intracellular non-heme Fe2+ and added DETC served as a trap for endogenously produced NO. The time-dependent changes of NO production were connected with the periodicity of liver regeneration. The first increase in NO production occurred ca. 1 h after partial hepatectomy (PHE). The second and more pronounced peak of NO production was observed about 6 h after PHE, when the hepatocytes entered the first cell cycle; it originated mainly from these cells. The following minimum of NO synthesis coincided with the maximal rate of DNA synthesis. The third gradual rise of NO production was seen at the end of the investigated period that covered the G2 + M phases, the transit from the first to the second cell cycle of the hepatocytes and the entrance of the nonparenchymal cells into proliferation.

Animals↗

PubMed1994

Anterograde neuronal tracing of retinohypothalamic projections in the hamster--possible innervation of substance P-containing neurons in the suprachiasmatic nucleus.

The retinohypothalamic tract (RHT) in the Djungarian hamster Phodopus sungorus was studied using anterograde neuronal transport of cholera toxin subunit B (CTB) following unilateral intraocular injection. A major projection terminates bilaterally in the hypothalamic suprachiasmatic nuclei (SCN). In the anterior ventral SCN, a light ipsilateral predominance was evident. In the medial SCN, labelling was concentrated laterally where it was seen over the dorso-ventral extension of the nuclei, pronounced contralaterally to the site of CTB injection, which was even more characteristic in the posterior aspects of the nuclei. Labelled fibers and terminals were observed in the supraoptic nuclei, but not in lateral and paraventricular hypothalamic regions. Additional experiments utilizing double immunofluorescence of CTB and of substance P (SP) in the SCN showed that SP-containing perikarya were particularly observed in a central portion of the nucleus, where CTB-stained terminals were accumulated in the vicinity of immunoreactive cell bodies, fibers and terminals. Our data provide preliminary morphological evidence for the regulation of SCN function by retinal afferents and may explain the circadian and photoperiodic fluctuations in the amount of SP in the SCN.

Animals↗

PubMed1994

Regulation of the mRNA expression for tumor necrosis factor-alpha in rat liver macrophages.

Kupffer cells are known to produce tumor necrosis factor-alpha upon stimulation with endotoxin or viruses. This tumor necrosis factor-alpha synthesis is suppressed by prostaglandin E2 or dexamethasone. Using Northern blotting and reverse transcriptase-polymerase chain reaction, it is demonstrated that endotoxin-induced tumor necrosis factor-alpha synthesis is blocked by prostaglandin E2 or dibutyryl 3':5'-cyclic adenosine monophosphate on the transcriptional level. Tumor necrosis factor-alpha itself suppressed endotoxin-evoked tumor necrosis factor-alpha mRNA expression when given in a narrow time interval with lipopolysaccharide. Interleukin-10 of human or mouse origin also inhibited the synthesis of tumor necrosis factor-alpha mRNA and protein when given more than 2 h prior to the endotoxin challenge. The suppressive effect of prostaglandin E2 lasted for more than 36 h while IL-10 blocked tumor necrosis factor-alpha production for barely 24 h. Dexamethasone reduced the endotoxin-induced tumor necrosis factor-alpha mRNA formation by approximately 50% only, although it led to nearly complete inhibition of the synthesis of the mature protein. Taken together with reverse transcriptase-polymerase chain reaction data revealing significant amounts of tumor necrosis factor-alpha mRNA in resting Kupffer cells, an additional posttranscriptional regulation of tumor necrosis factor-alpha synthesis has to be assumed. Tumor necrosis factor-alpha mRNA was not induced by interferon-gamma, interleukin-1 beta or interleukin-6 (the latter two cytokines are also synthesized by Kupffer cells), but a 24-h prestimulation of liver macrophages with interferon-gamma or phorbol ester had a modest priming effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effects of hypoxia on the oxygen-dependent metabolism of prostaglandins and adenosine in liver cells.

In this study, the capacity of hepatocytes to degrade prostaglandins diminished if the partial oxygen pressure dropped below 5%. This decrease was accompanied by an increased lactate/pyruvate ratio, a decrease in fatty acid oxidation and a drop in the ATP level. The degradation of exogenous adenosine increased with decreasing oxygen tension. At a partial oxygen pressure below 10%, the conversion of uric acid to allantoin, the final catabolite of adenosine in the rat, was strongly inhibited, resulting in the accumulation of uric acid in the medium. A good correlation was observed between the partial oxygen pressure, the oxidation of uric acid to allantoin and the degradation of prostaglandins D2 and E2, suggesting a peroxisomal pathway of hepatic prostaglandin oxidation. Subcellular fractionation of liver homogenates revealed peroxisomes as the site of degradation of prostaglandins D2 and E2 augmented by cytosolic components. The similarity of the degradation products found in the cell-free system, in hepatocytes and in the perfused liver further supports a peroxisomal degradation of prostaglandins in vivo. Stimulated liver macrophages (Kupffer cells) produced the same amount and pattern of eicosanoids at 1% and 21% O2. Even the formation of superoxide remained unaffected down to a partial pressure of 1%. At partial O2 pressures below 1%, the production of prostaglandins and superoxide became strongly inhibited. These results indicate that essential oxygenation reactions in activated Kupffer cells, including prostaglandin synthesis, possess high affinities to oxygen, while the peroxisomal pathway of prostaglandin oxidation in hepatocytes is sensitive to an O2 tension as low as 5%.

Adenosine↗

PubMed1994

Regulation of tumor necrosis factor-alpha-mRNA synthesis and distribution of tumor necrosis factor-alpha-mRNA synthesizing cells in rat liver during experimental endotoxemia.

Stimulated liver macrophages (Kupffer cells) are known to release a variety of inflammation-related substances, e.g. cytokines, prostanoids, and reactive oxygen intermediates. For instance, exposure of Kupffer cells in vitro to lipopolysaccharide (endotoxin) leads to a strongly enhanced synthesis of the mRNA for tumor necrosis factor-alpha, the release of the mature protein into culture media. These events are influenced by prostanoids and corticoid hormones. Kupffer cells are thought to be the only source of tumor necrosis factor-alpha within the hepatic sinusoid, but neither this cell specificity nor the regulatory influence of glucocorticoids or prostanoids has been confirmed in the intact organ. Using non-radioactive in situ hybridization, it was possible to obtain specific signals for tumor necrosis factor-alpha-mRNA in individual Kupffer cells uniformly distributed (as compared to Kupffer cells detected by immunohistochemistry) throughout the liver. Kupffer cells were the only cells in the hepatic sinusoids of lipopolysaccharide-perfused livers to express mRNA for tumor necrosis factor-alpha. Simultaneous addition of endotoxin plus dexamethasone and endotoxin and prostaglandin E2 completely suppressed the synthesis of this mRNA. Unexpectedly, the presence of mRNA for tumor necrosis factor-alpha was also detected in the intrahepatic bile duct epithelium of lipopolysaccharide-perfused livers. It is known that biologically active endotoxin is secreted via the bile ducts. These results seem to indicate that bile duct epithelium responds to inflammatory agents with synthesis of tumor necrosis factor-alpha-mRNA. One must also consider new functional aspects of bile duct epithelium in chronic inflammatory diseases, e.g. primary biliary cirrhosis, chronic sclerosing cholangitis or graft-versus-host disease.

Animals↗

PubMed1994

Regulation of interleukin-6 receptor expression in rat Kupffer cells: modulation by cytokines, dexamethasone and prostaglandin E2.

Interleukin-6 has a variety of biological effects, mainly on the immune system. The regulation of this signal at both the site of production and the site of action is necessary to maintain the organism's homeostasis. In the microenvironment of the hepatic sinusoids, Kupffer cells as resident macrophages are the most potent source of interleukin-6 during inflammation. This cytokine is an important signal to hepatocytes during the early stages of the acute-phase response, leading to the expression of several major plasma proteins. Kupffer cells were found to express interleukin-6 receptor constitutively. Interleukin-6 decreased the level of interleukin-6 receptor mRNA, indicating an autocrine pathway by which Kupffer cells regulate their responsiveness to interleukin-6. Furthermore, lipopolysaccharide, tumor necrosis factor-alpha, interferon-gamma, interleukin-1 beta and phorbol ester induced interleukin-6 production and, at the same time, suppressed the level of interleukin-6 receptor mRNA. The existence of an autocrine loop in rat Kupffer cells may be physiologically relevant, as it would contribute to a regulated interleukin-6 signal chain in the liver. The anti-inflammatory mediators dexamethasone or PGE2 and its second messenger, cyclic AMP, increased interleukin-6 receptor mRNA, whereas prostaglandin D2 or the Ca2+ ionophore, A 23187, were without effect. The changes in interleukin-6 mRNA were paralleled by the number of interleukin-6 receptors present on Kupffer cells as detected by binding of 125I-interleukin-6. These results suggest the existence of control mechanisms involving several soluble mediators that help balance the level of interleukin-6-R mRNA in rat liver macrophages.

Animals↗

PubMed1994

[Incidence and importance of Clostridium difficile in patients treated with antibacterial therapy or perioperative preventive cefoxitin administration].

Clostridium difficile and/or toxin B were isolated from the faeces of 3 (1.6%) of 184 patients within the first two days of hospitalisation in the University of Tübingen, Gynaecological Clinic. With following stool samples from a total of 117 patients the isolation rate of C. difficile was examined in relation to the treatment with antibiotics. From the first group of 61 patients, who had had gynaecological operations and were not treated with any antibiotic, the isolation rate of C. difficile rose statistically but not significantly from 0% at the time of admission up to 3.3% during hospitalisation. Amongst the second group of 17 patients, who had had gynaecological operations and were treated with various antibiotics for at least three days, the isolation rate was also found to rise insignificantly from 0 to 11.8% (p < 0.1). The third group of 33 patients, who had had gynaecological operations and perioperative prophylaxis with cefoxitin (one to three doses 2 g each), the isolation rate rose significantly from 0 to 12.1% (p < 0.05). The result of this study shows that the bacterial flora of the gut was probably altered even after a very brief application of cefoxitin. In two environmental examinations on the wards of the patients of this study, C. difficile was not isolated in any case.

Adult↗