Search

Background: Infectious complications remain a major clinical problem in colorectal surgery, contributing to prolonged hospital stays, additional costs and significant postoperative mortality. Presepsin has been reported to be a useful marker to diagnose sepsis, similar or superior to procalcitonin (PCT) and C-reactive protein (CRP), and plasma presepsin concentrations are associated with the severity of sepsis and its outcome. The aim of this study was to assess the diagnostic value of presepsin in the early detection of infectious complications after elective colorectal surgery, compared with CRP and PCT.Methods: This study was a prospective observational study. Patients of age >18 who underwent elective colon resections were enrolled and patients with end-stage kidney disease were excluded. Blood samples were collected just before surgery and on postoperative day (POD) 1, 2, 3, 4, and 6. Infectious complications were diagnosed by surgeons. Results: A total of 114 patients were examined, and 27 patients (23.7%) developed infectious complications: 11 anastomotic leaks, 13 intra-abdominal infections, and 3 wound infections. CRP and PCT markedly increased from POD1 to POD3 and then gradually decreased toward POD6 in both groups, but the trends of the decrease in the infected group were blunt, compared with those in the non-infected group. On the other hand, presepsin did not show major changes just after surgery, but it increased on POD4 and POD6, when the complications occurred. ROC analysis to predict infectious complications revealed that the best accuracy was obtained on POD 6 for all biomarkers. CRP showed excellent predictability and presepsin showed good predictability. However, the cut-off values of all biomarkers were relatively lower than expected. Conclusions: The trends of change in presepsin following colorectal surgeries were distinct from those of CRP and PCT. Monitoring the presepsin trends after colorectal surgeries could be helpful to detect postoperative infectious complications.Trial registration: UMIN000025313. Registered on 17 December 2016.

Considering previous data from our clinic, as had consistently demonstrated a significant number of OLP patients also reporting thyroid disease (Hashimoto's thyroiditis, in particular), the present study investigated the prevalence of OLP in patients with autoimmune thyroid disease, including Hashimoto's thyroiditis and Graves' disease.

This article reports a case of oral lichenoid contact reaction (OLCR) in which a bilateral lesion involving the buccal mucosa was observed. Its relevance lies on that the lesions could be misdiagnosed as an oral leukoplakia, since they showed a typical feature of a homogeneous white plaque; however, fortunately, this misjudgement was spared because one of the lesions, on the right-buccal side, was in direct contact with an amalgam filling. Hence, the suspicion of mucosal contact reaction was made and the patient successfully treated by amalgam replacement. Comments on diagnosing of OLCR is also included is this report.

As reações liquenoides por drogas são mais comuns na pele, mas também podem ocorrer na mucosa bucal. Estas lesões são de difícil diagnóstico por causa de sua semelhança clínica com às do líquen plano oral idiopático. O presente artigo relata um caso de reação liquenoide em mucosa bucal, associado ao uso de carbamazepina, no qual o processo de diagnóstico é enfatizado

This article reports a case in which a patient, an adult black male, was diagnosed as having sialadenosis of an idiopathic type, since clinical, computed tomography and laboratory examinations did not disclose any other abnormalities that could be associated with the glandular swelling. As this condition is quite harmless, requiring no intervention, unless for aesthetic reason, the patient was dismissed, being monitored sporadically. But after 8 months since the first consultation, the patient was diagnosed as having an advanced esophageal squamous cell carcinoma, and eventually died of this disease. This report, therefore, raises the question whether there was any relation with the sialadenosis and the esophageal carcinoma. This question is very speculative, but it stands as a notice for clinicians in future cases of idiopathic sialadenosis to evaluate the patient for an underlying malignant disease.

This is one of a series of statements discussing the utilization of GI endoscopy in common clinical situations. The Standards of Practice Committee of the American Society for Gastrointestinal Endoscopy prepared this text. In preparing this guideline, a MEDLINE literature search was performed and additional references were obtained from the bibliographies of the identified articles and from recommendations of expert consultants. When little or no data exist from well-designed prospective trials, emphasis is given to results from large series and reports from recognized experts. Guidelines for appropriate utilization of endoscopy are based on a critical review of the available data and expert consensus. Further controlled clinical studies are needed to clarify aspects of this statement, and revision may be necessary as new data appear Clinical consideration may justify a course of action at variance to these recommendations.

This is one of a series of statements discussing the utilization of GI endoscopy in common clinical situations. The Standards of Practice Committee of the American Society for Gastrointestinal Endoscopy prepared this text. In preparing this guideline, a MEDLINE literature search was performed, and additional references were obtained from the bibliographies of the identified articles and from recommendations of experts. When little or no data exist from well-designed prospective trials, emphasis is given to results from large series and reports from recognized experts. Guidelines for appropriate utilization of endoscopy are based on a critical review of the available data and expert consensus. Further controlled clinical studies are needed to clarify aspects of this statement and revision needed to clarify aspects of this statement and revision may be necessary as new data appear. Clinical consideration may justify a course of action at variance to the recommendations.

This is one of a series of statements discussing the utilization of GI endoscopy in common clinical situations. The Standards of Practice Committee of the American Society for Gastrointestinal Endoscopy prepared this text. In preparing this guideline, a MEDLINE literature search was performed, and additional references were obtained from the bibliographies of the identified articles and from recommendations of expert consultants. When little or no data exist from well-designed prospective trials, emphasis is given to results from large series and reports from recognized experts. Guidelines for appropriate utilization of endoscopy are based on a critical review of the available data and expert consensus. Further controlled clinical studies are needed to clarify aspects of this statement, and revision may be necessary as new data appear. Clinical consideration may justify a course of action at variance to these recommendations.

This is one of a series of statements discussing the utilization of GI endoscopy in common clinical situations. The Standards of Practice Committee of the American Society for Gastrointestinal Endoscopy prepared this text. In preparing this guideline, a MEDLINE literature search was performed, and additional references were obtained from the bibliographies of the identified articles and from recommendations of expert consultants. When little or no data exist from well-designed prospective trials, emphasis is given to results from large series and reports from recognized experts. Guidelines for appropriate utilization of endoscopy are based on a critical review of the available data and expert consensus. Further controlled clinical studies are needed to clarify aspects of this statement, and revision may be necessary as new data appear. Clinical consideration may justify a course of action at variance to these recommendations.

Obtaining an early indication of the quality of meat such as defective meat comprising the steps of taking a sample of muscle tissue, disrupting and incubating the sample in order to activate and progress the conversion of glycogen to lactic acid so that the conversion proceeds at a rapid rate by comparison to normal conversion rate in muscle tissue processed and stored normally in meat processing operations and providing an indication of the pH to determine if in range that indicates the meat is defective. A sampling tool (111) usable to sample a muscle tissue having a conical tool head (112) with a leading point (121) to aid insertion into an animal and rearwardly facing cutting edge (123) that takes a sample of tissue when the tool is being withdrawn. A sample removing means (127) having a front convex surface (128) able to force the sample out of a concave base (120) of the tool head (112).

Seizures, hemorrhage, neurogenic pulmonary edemas, and venous embolisms are all potential perioperative complications. Although they are not usually life-threatening, the anesthesiologist should be familiar with their pathophysiology, diagnosis, and treatment, all of which will be described in this chapter.

BACKGROUND We have previously found that agents increasing intracellular cAMP levels of smooth muscles, such as PDE3 inhibitors, aminophylline and prostaglandin E1, produce both bronchodilation and pulmonary vasodilation in serotonin-induced pulmonary hypertension and bronchoconstriction models. In the present study we have simultaneously evaluated the spasmolytic effects of colforsin daropate, a novel forskolin derivative, on serotonin-induced pulmonary hypertension and bronchoconstriction. METHODS Ten mongrel dogs were anesthetized with pentobarbital. The pulmonary hypertension and bronchoconstriction were elicited with serotonin (10 microg/kg + 1 mg x kg(-1) x h(-1)) and assessed as percentage changes in pulmonary vascular resistance (PVR) and bronchial cross-sectional area (BCA) (basal = 100%). Initially, the relaxant effects of colforsin daropate (0-300 microg/kg) were determined. The PVR and BCA were assessed before and 30 min after serotonin infusion began and 5 min after each dose of colforsin daropate. To determine whether colforsin daropate-induced relaxation is independent of plasma catecholamine, propranolol 0.4 mg/kg was given following colforsin daropate 300 microg/kg i.v. RESULTS Colforsin daropate reversed both pulmonary hypertension and bronchoconstriction dose-dependently: -logED50 (95% confidence intervals, mean ED50) for pulmonary hypertension and bronchoconstriction 5.44 (5.08-5.80, 3.6 microg/kg) and 4.90 (4.06-5.20, 12.5 microg/kg), respectively. However, colforsin daropate (>or= 30 microg/kg) produced a more pronounced systemic than pulmonary vasodilation. Although colforsin daropate (>or= 30 microg/kg) significantly increased plasma catecholamines, propranolol did not reverse the relaxant effects. CONCLUSIONS Colforsin daropate may attenuate bronchoconstriction and pulmonary hypertension. In addition, as beta-blockade did not change the attenuation, the relaxant effects may be independent of plasma catecholamines.

PURPOSE: Hormone replacement therapy (HRT) is typically withheld from women with breast cancer because of concern that it might increase the risk of recurrence. The purpose of this study was to quantify the risk of recurrent breast cancer associated with HRT among breast cancer survivors. METHODS: We performed a systematic literature review through May 1999, calculating the relative risk (RR) of breast cancer recurrence in each study by comparing the number of recurrences in the HRT group to those in the control group. In studies that did not contain a control group, we constructed one by estimating the expected number of recurrences based on data from the Early Breast Cancer Trialists’ Collaborative Group, adjusting for nodal status and disease-free interval. RRs across all studies were combined using random-effects models. RESULTS: Of the 11 eligible studies, four had control groups and included 214 breast cancer survivors who began HRT after a mean disease-free interval of 52 months. Over a mean follow-up of 30 months, 17 of 214 HRT users experienced recurrence (4.2% per year), compared with 66 of 623 controls (5.4% per year). HRT did not seem to affect breast cancer recurrence risk (RR = 0.64, 95% confidence interval [CI], 0.36 to 1.15). Including all 11 studies in the analyses (669 HRT users), using estimated control groups for the seven uncontrolled trials, the combined RR was 0.82 (95% CI, 0.58 to 1.15). CONCLUSION: Although our analyses suggest that HRT has no significant effect on breast cancer recurrence, these findings were based on observational data subject to a variety of biases.

BACKGROUND Magnesium (Mg2+) has relaxant effects on histamine-induced bronchoconstriction. In addition, Mg2+ has been reported to reduce vascular smooth muscle tone and be clinically useful for treatment of persistent pulmonary hypertension of the newborn. In this study, we evaluated the relaxant effect of Mg2+ on serotonin (5HT)-induced bronchoconstriction and pulmonary hypertension. METHODS Seven mongrel dogs were anesthetized with pentobarbital (30 mg x kg(-1) + 2 mg x kg(-1) x h(-1)) and paralyzed by pancuronium (0.2 mg x kg(-1) x h(-1)). Bronchoconstriction and pulmonary hypertension were elicited with 5HT (10 microg x kg(-1) + 1 mg x kg(-1) x h(-1)). Airway caliber was evaluated by changes in bronchial cross-sectional area (BCA) of the 3rd bronchial bifurcation measured by a fiberoptic bronchoscope method as previously reported. Pulmonary hypertension was assessed by changes in pulmonary vascular resistance (PVR). The BCA and PVR were expressed as per cent of the basal level. Thirty minutes after start of 5HT infusion, magnesium sulfate (MgSO4): 0 (saline), 1, 10, 100 and 1000 micromol x kg(-1) was given i.v.. Arterial blood was also collected to measure plasma level of Mg2+ and catecholamines. RESULTS 5HT increased %PVR to 163+/-25% and decreased % BCA by 39.2+/-4.5%. Plasma level of Mg2+ following MgSO4 1000 micromol x kg(-1) i.v. exceeded its toxic level. The ED50s of MgSO4 (dose producing 50% relaxation of maximal constriction) was 47.8 micromol x kg(-1) and 1.09 mmol x kg(-1) for pulmonary hypertension and bronchoconstriction, respectively. The ratio of %PVR to %SVR was about 1.0 after MgSO4 0-100 micromol x kg(-1) i.v., although the ratio significantly increased after 1000 micromol x kg(-1) i.v.. CONCLUSION In dogs, 5HT-induced pulmonary hypertension but not bronchoconstriction was significantly reduced by an iv bolus of MgSO4, resulting in a plasma concentration within the assumed therapeutic level.

Background & Aims: Adenocarcinoma of the esophagus and esophagogastric junction (EGJ) is increasing, the earliest lesion being specialized intestinal metaplasia (SIM). This study determined the prevalence and demographic features of patients with SIM, dysplasia, and cancer in the esophagus and EGJ. Methods: Two antegrade biopsy specimens were taken distal to the squamocolumnar junction (SCJ) and any tongues of pink mucosa proximal to the SCJ. Patients were categorized endoscopically and histologically as having long-segment (LSBE) or short-segment Barrett's esophagus (SSBE), EGJ-SIM, or a normal EGJ. Results: Of 889 patients studied, 56 were undergoing esophagoduodenoscopy screening or surveillance and were not included in the prevalence calculation. The overall prevalence of SIM was 13.2%, with 1.6% LSBE, 6.0% SSBE, and 5.6% EGJ-SIM. Dysplasia or cancer was noted in 31% of LSBE, 10% of SSBE, and 6.4% of EGJ-SIM patients ( P ≤ 0.043). Two cancers were associated with LSBE, 1 with SSBE, and 1 with EGJ-SIM. Patients with LSBE and SSBE were predominantly white ( P ≤ 0.001), male ( P ≤ 0.009), and smokers ( P ≤ 0.004), with LSBE patients having a longer history of heartburn ( P ≤ 0.009). In contrast, patients with EGJ-SIM were similar in gender and ethnicity to the reference group, tended to be older ( P ≤ 0.05), drank less alcohol ( P ≤ 0.02), and had a higher prevalence of Helicobacter pylori infection ( P ≤ 0.05). Conclusions: The prevalence of SSBE and EGJ-SIM is similar, but each entity is 3.5 times more prevalent than LSBE. However, the prevalence of dysplasia in LSBE is 2 times greater than in SSBE and 4 times greater than in EGJ-SIM. Demographically, EGJ-SIM patients are different from patients with Barrett's esophagus and have a higher prevalence of H.pylori infection. These data help to explain the increasing incidence of adenocarcinoma of the distal esophagus and EGJ. GASTROENTEROLOGY 1999;116:277-285

Background The authors examined the interaction of ketamine with recombinant mu, kappa, and delta opioid receptors and recombinant orphan opioid receptors expressed in Chinese hamster ovary cells (CHO-mu, CHO-kappa, CHO-delta, and CHO(ORL1), respectively). Methods CHO-mu, CHO-kappa, and CHO-delta membranes were incubated with the opioid receptor radioligand [3H]diprenorphine at room temperature. Ketamine (racemic, R(-) and S(+)) was included at concentrations covering the clinical range. CHO(ORL1) membranes were incubated with [125I]Tyr(14)nociceptin and racemic ketamine at room temperature. The effects of racemic ketamine and selective opioid receptor agonists (mu: [D-Ala2, MePhe4, Gly(ol)5] enkephalin (DAMGO); kappa: spiradoline or delta: [D-pen2, D-pen5] enkephalin (DPDPE)) on forskolin-stimulated cyclic adenosine monophosphate formation also were examined. Data are mean +/- SEM. Results Racemic ketamine increased the radioligand equilibrium dissociation constant for [3H]diprenorphine from 85+/-5 to 273+/-11, 91+/-6 to 154+/-16, and 372+/-15 to 855+/-42 pM in CHO-mu, CHO-kappa, and CHO-delta, respectively. The concentration of radioligand bound at saturation was unaffected. In CHO-mu and CHO-kappa cells, racemic ketamine did not slow the rate of naloxone-induced [3H]diprenorphine dissociation. Ketamine and its isomers also displaced [3H]diprenorphine binding to mu, kappa, and delta receptors in a dose-dependent manner, with pKi values for racemic ketamine of 4.38+/-0.02, 4.55+/-0.04, and 3.57+/-0.02, respectively. S(+)-ketamine was two to three times more potent than R(-)-ketamine at mu and kappa receptors. Racemic ketamine displaced [125I]Tyr(14)nociceptin with an estimated affinity constant of 0.5 mM. Racemic ketamine inhibited the formation of cyclic adenosine monophosphate (naloxone insensitive) in a dose-dependent manner (concentration producing 50% inhibition approximately 2 mM) in all cell lines, including untransfected CHO cells. Ketamine (100 microM) reversed DAMGO (mu) and spiradoline (kappa) inhibition of formation of cyclic adenosine monophosphate. Conclusions Ketamine interacts stereoselectively with recombinant mu and kappa opioid receptors.

The rat μ-opioid receptor has recently been cloned, yet its second messenger coupling remains unclear. The endogenous μ-opioid receptor in SH-SY5Y cells couples to phospholipase C (PLC), increases [Ca2+]i and inhibits adenylyl cyclase (AC). We have examined the effects of μ-opioid agonists on inositol(1,4,5)trisphosphate (Ins(1,4,5)P3), [Ca2+]i and adenosine 3′: 5′-cyclic monophosphate (cyclic AMP) formation in Chinese hamster ovarian (CHO) cells transfected with the cloned μ-opioid receptor. Opioid receptor binding was assessed with [3H]-diprenorphine ([3H]-DPN) as a radiolabel. Ins(1,4,5)P3 and cyclic AMP were measured by specific radioreceptor assays. [Ca2+]i was measured fluorimetrically with Fura-2. Scatchard analysis of [3H]-DPN binding revealed that the Bmax varied between passages. Fentanyl (10 pm–1 μm) dose-dependently displaced [3H]-DPN, yielding a curve which had a Hill slope of less than unity (0.6±0.1), and was best fit to a two site model, with pKi values (% of sites) of 9.97±0.4 (27±4.8%) and 7.68±0.07 (73±4.8%). In the presence of GppNHp (100 μm) and Na+ (100 mm), the curve was shifted to the right and became steeper (Hill slope=0.9±0.1) with a pKi value of 6.76±0.04. Fentanyl (0.1 nm–1 μm) had no effect on basal, but dose-dependently inhibited forskolin (1 μm)-stimulated, cyclic AMP formation (pIC50=7.42±0.23), in a pertussis toxin (PTX; 100 ng ml−1 for 24 h)-sensitive and naloxone-reversible manner (Ki=1.7 nm). Morphine (1 μm) and [d-Ala2, MePhe4, gly(ol)5]-enkephalin (DAMGO, 1 μm) also inhibited forskolin (1 μm)-stimulated cyclic AMP formation, whilst [d-Pen2, d-Pen5], enkephalin (DPDPE, 1 μm) did not. Fentanyl (0.1 nm–10 μm) caused a naloxone (1 μm)-reversible, dose-dependent stimulation of Ins(1,4,5)P3 formation, with a pEC50 of 7.95±0.15 (n=5). PTX (100 ng ml−1 for 24 h) abolished, whilst Ni2+ (2.5 mm) inhibited (by 52%), the fentanyl-induced Ins(1,4,5)P3 response. Morphine (1 μm) and DAMGO (1 μm), but not DPDPE (1 μm), also stimulated Ins(1,4,5)P3 formation. Fentanyl (1 μm) also caused an increase in [Ca2+]i (80±16.4 nm, n=6), reaching a maximum at 26.8±2.5 s. The increase in [Ca2+]i remained elevated until sampling ended (200 s) and was essentially abolished by the addition of naloxone (1 μm). Pre-incubation with naloxone (1 μm, 3 min) completely abolished fentanyl-induced increases in [Ca2+]i. In conclusion, the cloned μ-opioid receptor when expressed in CHO cells stimulates PLC and inhibits AC, both effects being mediated by a PTX-sensitive G-protein. In addition, the receptor couples to an increase in [Ca2+]i. These findings are consistent with the previously described effector-second messenger coupling of the endogenous μ-opioid receptor. British Journal of Pharmacology (1997) 120, 1165–1171; doi:10.1038/sj.bjp.0701012

We have examined the interaction of procaine, prilocaine, lignocaine, bupivacaine, amylocaine and R(+) and S(-) ropivacaine with L-type voltage-sensitive Ca2+ channels in rat cerebrocortical membranes. Membranes were prepared in Tris HCl 50 mmol litre-1, pH 7.4, by homogenization and centrifugation. Binding assays were performed in 1-ml volumes of Tris HCl 50 mmol litre-1, pH 7.4, for 90 min at room temperature using approximately 200 micrograms of protein. Non-specific binding was defined in the presence of nifedipine 10(-5) mol litre-1, and bound and free radioactivity were separated by vacuum filtration. The effects of local anaesthetics were determined by displacement of [3H]PN200-110 (approximately 0.2 nmol litre-1), a radiolabelled 1,4- dihydropyridine (DHP) L-channel antagonist. The concentration of displacer producing 50% displacement was corrected for the competing mass of [3H]PN200-110 to yield the affinity constant, K50. All local anaesthetics displaced [3H]PN200-110 in a dose-dependent manner with a rank order potency of (K50, mmol litre-1) bupivacaine (0.48), amylocaine (0.74), lignocaine (1.09), prilocaine (2.06) and procaine (2.09). Ropivacaine enantiomers did not show stereo-selective displacement, with K50 values of 0.99 and 0.92 mmol litre-1 for R(+) and S(-) ropivacaine, respectively. There was a significant correlation between pK50 and p (octanol:buffer partition coefficient) (r2 = 0.872, P = 0.020), pK50 and p (local anaesthetic potency) (r2 = 0.816, P = 0.036), pK50 and p (relative conduction blocking potency) (r2 = 0.843, P = 0.028) and between pK50 and p (IC50 for inhibition of cardiac output) (r2 = 0.897, P = 0.015). These data suggest that DHP binding sites may be involved in both the mechanism of local anaesthesia and the cardiotoxicity of these agents.

Radioligand binding studies using the L-type voltage sensitive Ca2+ channel (VSCC) antagonist (+)-[3H]PN200-110 revealed the following rank order channel density in rat brain and cultured neuronal cell homogenates: striatumor = cerebrocortexcerebellum = brainstemSH-SY5Y cell lineNG108-15 cell line1321N1 cell linePC12 cell line. There were no significant differences in the equilibrium dissociation constant, Kd for (+)-[3H]PN200-110 or pK50 for nifedipine. K+ depolarization in SH-SY5Y cells and NG108-15 cells evoked a biphasic and monophasic increase in [Ca2+]i. The L-type Ca2+ channel antagonist nifedipine (1 microM) produced a 66 and 87% inhibition of the K(+)-evoked rise in the peak and plateau phase [Ca2+]i in SH-SY5Y cells and abolished the monophasic response in NG108-15 cells. The L-channel activator S(-)Bay K 8644 (1 microM) enhanced the K(+)-evoked increase in [Ca2+]i in both cell lines. These data demonstrate a comparatively low density of L-VSCC in undifferentiated SH-SY5Y cells, NG108-15 cells, 1321N1 cells and PC12 cells that are functionally active in at least SH-SY5Y cells and NG108-15 cells.

In 15 elderly residents of an old-age home, we measured the total number of bacteria and the numbers of streptococci and staphylococci in the pharynx over 5 months. Seven residents received professional oral health care from dentists and dental hygienists and eight practiced oral care by themselves or together with a helper. During the 5 months, the total number of bacteria and the numbers of streptococci and staphylococci decreased (p0.01) in those who received professional care. In contrast, the total number of bacteria and the numbers of streptococci and staphylococci neither did not change or increased in those who did not receive professional care. These findings show that professional oral health care by dentists and dental hygienists can decrease the total number of bacteria and the numbers of streptococci and staphylococci in the pharynx of elderly people, which might prevent aspiration pneumonia.

The history of domestic horse (Equus caballus) cytogenetics dates from 1912 when Kirillow reported the diploid chromosome number to be between 20 and 34 in male horses (see Power 1990). Later, Krallinger (1931) and Makino (1942) reported the number to be 64. Although this provided the correct chromosome number, the prevailing uncertainty was ®nally cleared in 1959 by Rothfels and co-workers who con®rmed the correct chormosome number as 2n ˆ 64 (Rothfels et al. 1959). The horse has 13 pairs of metacentric/submetacentric and 18 pairs of acrocentric autosomes. The X chromosome is the second largest submetacentric, while the Y chromosome is one of the smallest acrocentrics. During the 1970s, G-, Q-, C-, Rand NOR banding techniques were applied to horse chromosomes, and several arrangements of the chromosomes into a karyotype were presented (see Power 1990). The First International Conference for the Standardization of Banded Karyotypes of Domestic Animals held at Reading, UK, 1976, proposed a G-banded horse karyotype (the Reading Standard) with eight rows of chromosomes (Ford et al. 1980). Biarmed autosomes were arranged by decreasing length in the ®rst four rows. Acrocentrics were similarly arranged in the next three rows. The last row had only the sex chromosomes. This standard karyotype was used for several years. The lack of complete consensus among horse cytogeneticists led to a new standard (the Paris Standard) de®ned in 1989 (Richer et al. 1990). The chromosomes were arranged into two groups ± nonacrocentrics and acrocentrics. Within each group the chromosomes were ordered by length. The sex chromosomes were placed in the middle of the karyotype, along with the smallest biarmed chromosomes. C-, Rand NOR banded karyotypes were also presented. The Paris standard karyotype was more compact, with relatively better band resolution than the Reading Standard. Despite acceptance of the Paris Standard, the quality of the published banded images was a matter of concern. Furthermore, idiograms, band numbers and landmark descriptions were not provided, limiting the use of the standard to chromosome identi®cation only. The need for schematic drawings and band designations became particularly obvious in 1988 with the ®rst reports of physical gene mapping in horses (MHC: Ansari et al. 1988, MaEkinen et al. 1989; CRC: Harbitz et al. 1990; GPI: Chowdhary et al. 1992; PGD: Gu et al. 1992). Even though G-band idiograms and band descriptions (Maciulus et al. 1984) were available before these mapping efforts, dif®culties were encountered in the precise de®nition of the band locations primarily because of the lack of consensus on landmarks and band numbers. Development of the physical and genetic Chromosome Research 1997, 5, 433±443

To trace the fate of individual pollen grains through pollination processes, we determined genotypes of single pollen grains deposited on Hemerocallis stigmas in an experimental mixed-species array. Hemerocallis fulva, pollinated by butterflies, has diurnal, reddish and unscented flowers, and H. citrina, pollinated by hawkmoths, has nocturnal, yellowish and sweet scent flowers. We observed pollinator visits to an experimental array of 24 H. fulva and 12 F2 hybrids between the two species (H. fulva and H. citrina) and collected stigmas after every trip bout of swallowtail butterflies or hawkmoths. We then measured selection by swallowtail butterflies or hawkmoths through male and female components of pollination success as determined by single pollen genotyping. As expected, swallowtail butterflies imposed selection on reddish color and weak scent: the number of outcross pollen grains acquired is a quadratic function of flower color with the maximum at reddish color, and the combined pollination success was maximal at weak scent (almost unrecognizable for human). This explains why H. fulva, with reddish flowers and no recognizable scent, is mainly pollinated by swallowtail butterflies. However, we found no evidence of hawkmoths-mediated selection on flower color or scent. Our findings do not support a hypothesis that yellow flower color and strong scent intensity, the distinctive floral characteristics of H. citrina, having evolved in adaptations to hawkmoths. We suggest that the key trait that triggers the evolution of nocturnal flowers is flowering time rather than flower color and scent.

The mechanism by which racemic (R(+/-)) ketamine relaxes airway smooth muscle is unclear and there is no information on the differential effects of ketamine and its isomers. In this study, we have examined the spasmolytic effect of R(+/-) ketamine and its isomers S(+) and R(-) ketamine and the role of intracellular calcium and opioid receptors in R(+/-) ketamine-induced relaxation. The tension of isolated guinea pig tracheal strips was measured isometrically with a force displacement transducer and contraction elicited with histamine 10(-5) mol litre-1. In histamine-preconstricted strips, the two ketamine isomers (4.5-18.0 x 10(-4) mol litre-1) produced equipotent relaxation. A subthreshold dose of each isomer of ketamine (10(-4) mol litre-1) which alone did not relax histamine-induced contraction (S(+), P0.01; R(+/-), P0.01; R(-), P0.05) significantly potentiated adrenaline 1.25-5.0 x 10(-9) mol litre-1-induced relaxation (potency: S(+)R(+/-)R(-)). Increase in extracellular Ca2+ (1.8-14.4 x 10(-3) mol litre-1) significantly reduced R(+/-) ketamine-induced relaxation. S(-) Bay K 8644, at concentrations up to 2.0 x 10(-6) mol litre-1, partially antagonized R(+/-) ketamine-induced relaxation whereas at 10(-5) mol litre-1 or higher it potentiated the response. Naloxone 1.5-6.0 x 10(-6) mol litre-1 did not affect the relaxation caused by R(+/-) ketamine. We conclude that although both ketamine isomers produced equipotent spasmolytic effects on airway smooth muscle precontracted with histamine, they differed in their ability to potentiate the relaxing effect of adrenaline. S(+) ketamine produced the greatest potentiation. Changes in intracellular Ca2+ level secondary to a reduction in the L-type Ca2+ current may partially mediate the spasmolytic effect of R(+/-) ketamine.

As ketamine has local anaesthetic actions and local anaesthetics are known to have anti-inflammatory effects, ketamine could be expected to be an anti-inflammatory agent. Here we sought to determine whether ketamine is indeed anti-inflammatory in chemical peritonitis induced by HCl in rats.Peritonitis was elicited by applying 0.02 M HCl on the surface of the cecum or appendix and quantified by measuring the extravasation of intravenously injected Evan's Blue bound to albumin extracted from those tissues. Three experimental sets were performed. In the first set, four groups of 10 rats each received: 1%, 2%, and 4% ketamine and 1% lidocaine. In the same animal, before induction of peritonitis one area was topically pre-treated with 0.9% saline (control site) and another area was topically pre-treated with 1%, 2% or 4% ketamine or 1% lidocaine (experimental site). In the second set, two groups of 10 rats each received: 2% ketamine or 1% lidocaine. Ten min after the induction of peritonitis, the control site was topically treated with 0.9% saline, while the experimental site was treated with 2% ketamine or 1% lidocaine. In the third set 20 rats, divided into two groups, were pre-treated either with 2% S(+)ketamine or 2% R(-)ketamine before the induction of peritonitis instead of the previously employed racemic version of the drug.Treatment of the cecum or appendix areas with ketamine or lidocaine before the induction of peritonitis decreased the extravasation of Evan's Blue-albumin from 5.7 +/- 0.7 micrograms/100 mg tissue to 4.5 +/- 0.8, N.S. with 1% ketamine; from 5.9 +/- 0.8 to 4.1 +/- 0.7, P0.01 with 2% ketamine; from 4.8 +/- 0.7 to 3.5 +/- 0.6, P0.05 with 4% ketamine and from 5.9 +/- 0.6 to 3.6 +/- 0.8, P0.01 with 1% lidocaine. Treatment of the areas of peritonitis with 2% ketamine or 1% lidocaine decreased the extravasation of Evan's Blue-albumin from 5.6 +/- 0.5 micrograms/100 mg tissue to 4.4 +/- 0.6, P0.05 and from 6.0 +/- 0.8 to 5.0 +/- 0.7, P0.01. Administration of the isomer S(+)ketamine to colonic areas before the induction of peritonitis reduced the extravasation of Evan's Blue-albumin from 6.5 +/- 0.7 micrograms/100 mg tissue to 4.1 +/- 0.6, P0.01; while the isomer R(-)ketamine was inactive.These results indicate that topically applied ketamine inhibited the development of chemical peritonitis. This action of racemic ketamine was due to the isomer S(+)ketamine.

We investigated the effect of recombinant human IL-6 (rhlL-6) on cell proliferation using the MtT/E rat pituitary tumor cell line, which was recently established by Inoue et al. This cell line expresses the homeodomain protein Pit-1/GHF 1 and does not produce any significant amount of pituitary hormones, but retains its tumorigenicity by back-transplantation into rats, resulting in production of prolactin. MtT/E cells were seeded into Falcon 24-well plates at a density of 2×104 cells/well in a cultured medium, containing 10% horse serum and 2.5% fetal bovine, with test drug. After four-days (12 days for the time-course study) incubations, the cells were counted using a hemocytometer. Incubation for 4 days with rhlL-6 caused concentration-dependent stimulation of MtT/E cell growth and [3H]-thymidine incorporation into MtT/E cells. Addition of 20 ng/ml rhlL-6 to the culture medium stimulated MtT/E cell growth in a time-dependent manner, withdrawal of rhlL-6 from the culture medium reduced MtT/E cell growth, and re-addition of rhlL-6 to the culture medium again stimulated MtT/E cell growth. Among the cytokines tested, granulocyte colony-stimulating factor (rh G-CSF) also showed a slight but significant mitogenic activity on the MtT/E cells. Analysis of 125|-rhlL-6 binding to the MtT/E cells indicated a dissociation constant of 0.953×10−9 mmol/l and the presence of 968 binding sites per cell. These results confirm the previous finding that IL-6 exerts mitogenic activity on pituitary tumor cells and also support the hypothsis that IL-6 may be involved in the control of cell growth and proliferation in the pituitary.

This is one of a series of statements discussing the utilization of GI endoscopy in common clinical situations. The Standards of Practice Committee of the American Society for Gastrointestinal Endoscopy prepared this text. In preparing this guideline, a MEDLINE literature search was performed, and additional references were obtained from the bibliographies of the identified articles and from recommendations of expert consultants. When little or no data exist from well-designed prospective trials, emphasis is given to results from large series and reports from recognized experts. Guidelines for appropriate utilization of endoscopy are based on a critical review of the available data and expert consensus. Further controlled clinical studies are needed to clarify aspects of this statement, and revision may be necessary as new data appear. Clinical consideration may justify a course of action at variance to these recommendations.

The initial objective of this study was to establish a placental cell culture system in which the secretion of mouse growth hormone-releasing factor (mGHRF) could be examined during a several-day period. To determine when during pregnancy placental cells begin to express mGHRF, Northern blot analysis was carried out on total RNA from placentas collected on Days 6, 9, 11, 13, 15, 17, and 18 of pregnancy. Mouse GHRF mRNA could be detected as early as Day 11 of pregnancy. Its steady-state levels increased to maximum values on Days 15-17 and then declined slightly on Day 18. Placentas from Day 12 of pregnancy were selected for cell culture. The basal zone and labyrinth were dispersed in collagenase, and the cells were fractionated on a Percoll gradient. Two bands of cells were selected for further study. Both released significant amounts of immunoreactive mGHRF during a 5-day culture period. Effects of prolonged exposure of the cells to 8-bromo-cAMP and to agents that elevate intracellular cAMP concentration were then examined. Treatment of the cells with 0.5 mM 8-bromo-cAMP resulted in a significant decrease in the mGHRF concentration of the medium by the second day of culture. Mouse GHRF secretion was also inhibited by treatment of the cells with 100 ng/ml cholera toxin or 0.1 mM forskolin. The effect of 8-bromo-cAMP was concentration-dependent, with 0.1 mM being the lowest concentration that was active. 8-Bromo-cAMP treatment also reduced the steady-state level of mGHRF mRNA in the cells. These data demonstrate that mouse placental cells secrete mGHRF for at least 5 days in vitro, and they suggest that mGHRF gene expression in the placenta is regulated by intracellular cAMP concentration.

We investigated the possibility of detection of CINC/gro, which is a IL-8-like neutrophil chemoattractant, immunoreactivity in rat normal anterior pituitary gland by immunohistochemistry, western blot analysis and an ELISA. We first ascertained the possibility of detection of CINC/gro immunoreactivity in the anterior pituitary gland by immunocytochemistry. In the anterior lobe of the pituitary gland, a few CINC/gro-like immunoreactive cells were observed (1-3% of all cells in the anterior pituitary). The positive cells were middle or large in size and looked angular in shape. Intense immunoreactivity was observed in the cytoplasm but not in the nucleus. Analysis by immunoblotting with anti-CINC/gro antiserum gave a characteristic single CINC/gro band with a molecular weight of 6.3 kDa. CINC/gro immunoreactivity was also detected in 3-h conditioned medium of normal anterior pituitary cells by an ELISA, and that immunoreactivity increased significantly in a time-dependent manner during 24-h incubation. This immunoreactivity could be induced by TNF-α in a dose-dependent manner. These findings indicate that CINC/gro is produced in pituitary gland and also suggests the possibility that CINC/gro may play some role asa modulator of anterior pituitary function, especially in the cross-talk mechanism between the immune and neuroendocrine systems

The effect of vagotomy and sympathectomy on cardio-acceleratory and arterial hypertensive reflexes evoked by electrical stimulation of the rat glossopharyngeal (IXth) nerve was studied in relation to changes in baseline heart rate and arterial blood pressure. Uni- and bi-lateral transection of the cervical vagal trunk brought about augmentation of baseline heart rate, accompanied by a depression in reflex tachycardia; the amount of depression being inversely related to that of an increase in baseline heart rate. The latter increased more after a right vagotomy than after a left vagotomy. No appreciable change in reflex hypertension as well as in baseline blood pressure was observed by different types of vagotomy. For unilateral sympathectomy, semilunar cordotomy caudal to the obex was performed. It was found that right semilunar cordotomy significantly depressed the magnitude of cardio-acceleratory and arterial hypertensive reflexes in association with a significant decrease in baseline heart rate, though there was a less pronounced decrease in baseline blood pressure. The result obtained by a left semilunar cordotomy was similar to that of a right semilunar cordotomy, except that the decrease in reflex tachycardia was very small and statistically insignificant. Thus, the efferent activities in vagus and sympathetic nerves were more effective on the right than on the left side, in modifying reflex tachycardia and baseline heart rate, whereas, right and left sympathetic efferent outflows were equally effective in depressing the reflex increase in blood pressure.

A monoclonal antibody (mAb h-448) was prepared after cell fusion of mouse myeloma cells (SP2/0-Ag-14) to the spleen cells of mice immunised with serotype h strain (MF25) of Streptococcus downei. The antibody (IgM class) reacted in enzyme immunoassay only with whole cells as well as purified polysaccharide (PS) antigen of Streptococcus sobrinus (types d and g) and Streptococcus downei (serotype h), but not with cells or purified PS antigen from any other serotypes of the mutans group of streptococci. mAb h-448 also quantitatively precipitated in solution with the purified antigens. Competitive hapten inhibition tests demonstrated that beta-methylgalactopyranoside inhibited the reaction most strongly. Although rhamnose also showed a substantial inhibitory effect, the results of this study indicate that the antigenic determinant of the PS antigen has a structure similar to the beta-methylgalactopyranoside molecule.

Two hybridomas producing monoclonal antibodies (MAbs) were prepared by fusing myeloma cells (Sp2/0-Ag14) with mouse spleen cells immunized with purified spirosin from Yersinia enterocolitica SYT-11-72 (YE72). The antibodies produced by them were designated MAbs-S5 and S27. They were IgG2a and IgG1, respectively, both with kappa light chains. MAbs-S5 and S27 reacted specifically with spirosin from YE72. On Western blotting after limited proteolysis with Staphylococcus aureus V8 protease, YE72 spirosin revealed peptide fragments of 35 and 37 kDa reacting markedly with MAb-S5, which suggested the presence of an antigenic determinant on these fragments. By cellular fractionation of YE72 and subsequent EIA and Western blot analysis, spirosome was shown to be present in the cytoplasm of YE72.

Streptococcus mutans (S. mutans) をラットに1回静注し，増殖性糸球体腎炎を惹起することができた。 S. pyogenesと共通する多糖体抗原に対する抗体の存在下ではより強い腎病変が認められた。腎炎は免疫複合体型の機序により生ずるものと考えられ，両菌の共通多糖体抗原が腎炎発症に関与している可能性が示唆された。

Background Central noradrenergic neurones have a role in alertness, analgesia, and thermoregulation; these neurones are also involved in the mechanism of anaesthesia. Locus coeruleus neurones innervate various central nervous regions including the cerebral cortex and hippocampus, and are responsible for wakefulness and analgesia. We hypothesized that these neurones are also involved in both activation of the γ-aminobutyric acid type A (GABAA) receptor and inhibition of N-methyl- d -aspartate (NMDA) receptor-mediated anaesthesia. Methods Forty-seven male rats were used to compare duration of anaesthesia before and 10 days after noradrenergic neurone depletion after intraperitoneal (i.p.) administration of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4; 0, 5, and 50 mg kg−1). The animals received i.p. thiopental (GABA anaesthetic, 45 mg kg−1) or ketamine (NMDA anaesthetic, 100 mg kg−1). We also tested the effects of coerulean noradrenergic neurone depletion on i.p. ketamine analgesia (15 mg kg−1) using the hot-plate test in a further 21 male rats. At the end of each experiment, norepinephrine contents in the cerebral cortex and hippocampus were measured. Results I.P. DSP-4 5 and 50 mg kg−1 significantly decreased ketamine anaesthesia duration by 12.7% and 22.4%, increased thiopental anaesthesia duration by 10.8% and 24.5%, and reduced ketamine-increased hot-plate latency by 55.2% and 68.1%, respectively. In addition, i.p. DSP-4 5 and 50 mg kg−1 significantly reduced norepinephrine contents in coerulean brain regions by ∼20% and ∼75%, respectively. There were significant correlations between norepinephrine contents in coerulean brain regions and anaesthesia durations and ketamine analgesia. Conclusions The present data indicate that coerulean noradrenergic neurones may be responsible for both GABA- and NMDA-mediated anaesthetic actions.

Objectives: To investigate whether daily systemic and/or topical medication contributes to the development of oral lichen planus (OLP) lesions. Study Design: The study involved 110 OLP patients and 76 control subjects, matched by age, race and sex. The analyzed data included medical records, drug intake and topical medication. Criteria for analysis of drug intake included: (1) ATC-code drug classification; (2) number of different drugs used daily in the categories of monopharmacy (1 drug), minor polypharmacy (2 4 drugs), and major polypharmacy (> 5 drugs); and (3) drugs implicated in lichenoid reactions (DILRs). Results: Sixty (54.5%) of the 110 OLP patients reported daily medication (prior to the appearance of the OLP lesion) compared to 52 (68.4%) of the 76 control subjects. No statistical difference was found between the two groups in terms of systemic diseases, number of medicated individuals in the categories of mono- and polypharmacy, nor use of DILRs (P > 0.05). Regarding the clinical forms and site of involvement, a statistically significant difference was only found for the clinical erosive form of OLP, seen more frequently in non-DILR (P = 0.04) and nonmedicated OLP patients (P = 0.02) than in DILR OLP patients. Daily use of topical oral medication was reported by 2 (1.8%) OLP patients and 1 (1.3%) control subject. Conclusions: It seems that the use of systemic medication does not lead to a significant increase in the incidence of OLP lesions. For their part, lichenoid drug reactions are likely to occur only in a very low percentage of patients. © Medicina Oral S. L.