Visualization and quantification of anastomotic perfusion in colorectal surgery using near-infrared fluorescence.

BACKGROUND: Anastomotic leakage (AL) is one of the most troublesome complications in colorectal surgery. Recently, near-infrared fluorescence (NIRF) imaging has been used intraoperatively to detect sentinel lymph nodes and visualize the blood supply at the region of interest (ROI). The aim of this study was to evaluate the role of visualization and quantification of bowel perfusion around the anastomosis using NIRF system in predicting AL. METHODS: A prospective study was conducted on patients who had laparoscopic surgery for colorectal cancer at our institution. Perfusion of the anastomosis was evaluated with NIRF imaging after intravenous injection of indocyanine green (ICG). The time course of fluorescence intensity was recorded by an imaging analyzer We measured the time from ICG injection to the beginning of fluorescence (T0), maximum intensity (Imax), time to reach Imax (Tmax), time to reach Imax 50% ([Formula: see text]) and slope (S) after the anastomosis. RESULTS: Tumor locations were as follows; cecum: 2, ascending colon: 2, transverse colon: 7, descending colon: 1, sigmoid colon: 2, rectosigmoid colon: 3 and rectum: 6 (one case with synchronous cancer). All operations were performed laparoscopically. Four patients were diagnosed with or suspected to have AL (2 patients with grade B anastomotic leakage after low anterior resection, 1 patient with minor leakage in transverse colon resection and 1 patient needing re-anastomosis intraoperatively in transverse colon resection). T0 was significantly longer in the AL group than in patients without AL (64.3 ± 27.6 and 18.2 ± 6.6 s, p = 2.2 × 10-3). CONCLUSIONS: Perfusion of the anastomosis could be successfully visualized and quantified using NIRF imaging with ICG. T0 might be a useful parameter for prediction of AL.

Risk factors for neutropenia with lenalidomide plus dexamethasone therapy for multiple myeloma.

Neutropenia may develop as an adverse event in patients with multiple myeloma receiving lenalidomide (LEN) plus dexamethasone (DEX) therapy. In the present study, we examined the risk factors associated with grade 3/4 neutropenia during the first cycle of LEN plus DEX therapy. We observed that hemoglobin level (≤ 8.5 g/dl) was a significant risk factor for grade 3/4 neutropenia during the first cycle of therapy (odds ratio: 19.40; 95% confidence interval: 2.68-141.00; p < 0.01). thus, our findings suggest that determining the hemoglobin level could be useful in the risk management for neutropenia in patients receiving LEN plus DEX therapy.

CHIPS for genetic testing to improve a regional clinical genetic service.

In current practice of clinical genetics, molecular diagnosis has become more widely used than ever before. DNA diagnosis is important for appropriate medical care of the patient, and proper genetic counseling to the family. However, genetic testing of orphan disease cannot always be performed easily. In multiple congenital anomalies (MCA) syndromes by monogenic cause, the broad mutational spectrum and large size of responsible genes often make molecular diagnosis expensive and cumbersome. We solve this problem with on-demand genetic testing by CHIPS (CEL nuclease mediated heteroduplex incision with polyacrylamide gel electrophoresis and silver staining) technology, which is the ultimately conventional and economical mutation screening system. In this article, we show eight patients with MCA syndromes who were recently treated at our hospital, and demonstrate that CHIPS successfully offers efficient and inexpensive genetic testing and facilitates clinical genetic service in our local region.

Randomized clinical trial of defaecatory function after anterior resection for rectal cancer with high versus low ligation of the inferior mesenteric artery.

BACKGROUND: Defaecatory function is often poor after anterior resection. Denervation of the neorectum following high ligation of the inferior mesenteric artery (IMA) is a possible cause of impaired defaecatory function. The purpose of this randomized clinical trial was to clarify whether the level of ligation of the IMA in patients with rectal cancer affects defaecatory function. METHODS: Between 2008 and 2011, patients who underwent anterior resection for rectal cancer were randomized to receive either high or low ligation of the IMA. The primary endpoint was to demonstrate the superiority of low ligation in terms of defaecatory function. RESULTS: One hundred patients were enrolled in the study; 51 were randomized to high ligation of the IMA and 49 to low ligation. There were no differences between the groups in terms of clinical data, except tumour stage, which was more advanced in the high-ligation group (P = 0·046). Nor were there any differences in defaecatory function, self-assessment of defaecation, Faecal Incontinence Quality of Life scale or continence score between groups at 3 months and 1 year. The number of harvested lymph nodes was similar. The rate of symptomatic anastomotic leakage was 16 per cent in the high-ligation group and 10 per cent in the low-ligation group (P = 0·415). CONCLUSION: The level of ligation of the IMA in patients with rectal cancer did not affect defaecatory function or the incidence of postoperative complications. REGISTRATION NUMBER: NCT00701012 (http://www.clinicaltrials.gov).

Predicting the Readmission and Mortality in Older Patients Hospitalized with Pneumonia with Preadmission Frailty.

BACKGROUND: In older people, frailty has been recognized as an important prognostic factor. However, only a few studies have focused on multidimensional frailty as a predictor of mortality and readmission among inpatients with pneumonia. OBJECTIVE: The present study aimed to assess the association between preadmission frailty and clinical outcomes after the hospitalization of older patients with pneumonia. DESIGN: Single-center, retrospective case-control study. SETTING: Acute phase hospital at Kobe, Japan. PARTICIPANTS: The present study included 654 consecutive older inpatients with pneumonia. MEASUREMENTS: Frailty status before admission was assessed using total Kihon Checklist (KCL) score, which has been used as a self-administered questionnaire to assess comprehensive frailty, including physical, social, and cognitive status. The primary outcome was a composited 6-month mortality and readmission after discharge. RESULTS: In total, 330 patients were analyzed (median age: 79 years, male: 70.4%, median total KCL score: 10 points), of which 68 were readmitted and 10 died within 6 months. After multivariate analysis, total KCL score was associated with a composited 6-month mortality and readmission (adjusted hazard ratio, 1.07; 95% confidence interval, 1.02-1.12; p = 0.006). The cutoff value for total KCL score determined by receiver operating characteristic curve analysis was 15 points (area under the curve = 0.610). The group with a total KCL score ≥ 15 points had significantly higher readmission or mortality rates than the groups with a total KCL score < 15 points (p < 0.001). CONCLUSIONS: Preadmission frailty status in older patients with pneumonia was an independent risk factor for readmission and survival after hospitalization.

Cross talk between interferon-gamma and -alpha/beta signaling components in caveolar membrane domains.

Definition of cellular responses to cytokines often involves cross-communication through their respective receptors. Here, signaling by interferon-gamma (IFN-gamma) is shown to depend on the IFN-alpha/beta receptor components. Although these IFNs transmit signals through distinct receptor complexes, the IFN-alpha/beta receptor component, IFNAR1, facilitates efficient assembly of IFN-gamma-activated transcription factors. This cross talk is contingent on a constitutive subthreshold IFN-alpha/beta signaling and the association between the two nonligand-binding receptor components, IFNAR1 and IFNGR2, in the caveolar membrane domains. This aspect of signaling cross talk by IFNs may apply to other cytokines.

Reg IV is a serum biomarker for gastric cancer patients and predicts response to 5-fluorouracil-based chemotherapy.

Regenerating gene family, member 4 (Reg IV), a secreted protein, is overexpressed in several cancers, including gastric cancer (GC). In the present study, we measured Reg IV levels in sera from patients with GC by enzyme-linked immunosorbent assay. We also examined the effect of forced Reg IV expression on the apoptotic susceptibility to 5-fluorouracil (5-FU). Forced expression of Reg IV inhibited 5-FU-induced apoptosis. Induction of Bcl-2 and dihydropyrimidine dehydrogenase was involved in inhibition of apoptosis. Among 36 GC patients treated with a combination chemotherapy of low-dose 5-FU and cisplatin, all 14 Reg IV-positive patients showed no change or disease progression. The serum Reg IV concentration was similar between healthy individuals (mean+/-s.e., 0.52+/-0.05 ng/ml) and patients with chronic-active gastritis (0.36+/-0.09 ng/ml). However, the serum Reg IV concentration in presurgical GC patients was significantly elevated (1.96+/-0.17 ng/ml), even at stage I. The diagnostic sensitivity of serum Reg IV (36.1%) was superior to that of serum carcinoembryonic antigen (11.5%) or carbohydrate antigen 19-9 (13.1%). These results indicate that expression of Reg IV is a marker for prediction of resistance to 5-FU-based chemotherapy in patients with GC. Serum Reg IV represents a novel biomarker for GC.

Systematic search for gastric cancer-specific genes based on SAGE data: melanoma inhibitory activity and matrix metalloproteinase-10 are novel prognostic factors in patients with gastric cancer.

Gastric cancer (GC) is one of the most common malignancies worldwide. Genes expressed only in cancer tissue will be useful molecular markers for diagnosis and may also be good therapeutic targets. However, little is known about cancer-specific genes, at least in GC. In this study, we searched for GC-specific genes by serial analysis of gene expression (SAGE) data analysis and quantitative reverse transcription (RT)-PCR. Comparing GC SAGE libraries with those of various normal tissues in the SAGEmap database, we identified 54 candidate GC-specific genes. Quantitative RT-PCR analysis of these candidates revealed that APin protein (APIN), taxol resistance-associated gene 3 (TRAG3), cytochrome P450, family 2, subfamily W, polypeptide 1 (CYP2W1), melanoma inhibitory activity (MIA), matrix metalloproteinase-10 (MMP-10), dickkopf homolog 4 (DKK4), GW112, regenerating islet-derived family, member 4 (REGIV), and HORMA domain-containing 1 (HORMAD1) were expressed much more highly in GC than in 14 kinds of normal tissues. Immunohistochemical staining for MIA, MMP-10, and DKK4 was found in 47 (31.1%), 68 (45.0%), and two (1.3%) of 151 GCs, respectively, and staining for both MIA and MMP-10 was correlated with poor prognosis in advanced GC (P=0.0001 and 0.0141, respectively). Moreover, enzyme-linked immunosorbent assay showed high levels of MMP-10 (65/69, 94.2%) in serum samples from patients with GC. Levels of MIA were raised in a small proportion of serum samples from patients with GC (4/69, 5.8%). In Boyden chamber invasion assays, MIA-transfected GC cells were up to three times more invasive than cells transfected with empty vector. Taken together, these results suggest that MMP-10 is a good marker for the detection of GC and that MIA and MMP-10 are prognostic factors for GC. As expression of MIA and MMP-10 is narrowly restricted in cancer, these two molecules may be good therapeutic targets for GC.

A novel mechanism of cation/substrate cotransport: Na+/H+/adenosine cotransport in Vibrio parahaemolyticus.

Adenosine is actively transported with Na+ in Vibrio parahaemolyticus (Sakai, Y., Tsuda, M., Tsuchiya, T. (1987) Biochim, Biophys. Acta 893, 43-48). The proton conductor carbonylcyanide m-chlorophenylhydrazone, CCCP, strongly inhibited active transport of adenosine at pH 8.5 as well as at pH 7.0. This seemed peculiar because the driving force, an electrochemical potential of Na+, is established by the Na(+)-extruding respiratory chain at pH 8.5 in this organism, although it is established by the function of the Na+/H+ antiporter at pH 7.0. This suggested that H+ might be involved in the adenosine transport. We detected H+ uptake induced by adenosine influx in V. parahaemolyticus cells in the presence of Na+, but not in its absence, suggesting the occurrence of Na+/H+/adenosine cotransport. We isolated formycin A-resistant mutants which showed defective adenosine transport. The mutation resulted in simultaneous losses of Na+ uptake and H+ uptake induced by adenosine. In revertants from these mutants the Na+ uptake and H+ uptake were restored simultaneously. The frequencies of reversion were in the order of 10(-7), indicating that the mutations were single mutations; namely that Na+/adenosine cotransport and H+/adenosine cotransport took place via the same carrier. Thus, we conclude that adenosine is transported by the novel mechanism of Na+/H+/adenosine cotransport in V. parahaemolyticus.

Clinical course of silent thyroiditis in a patient with Sjögren's syndrome. Concomitant changes of antithyroid antibodies and antinuclear antibody.

A 68-year-old woman with Sjögren's syndrome simultaneously experienced thyrotoxicosis with a marked depression of thyroid radioactive iodine uptake and systemic lupus erythematosus-like symptoms, which both resolved spontaneously. Titers of antinuclear antibody and anti-DNA antibody were most elevated when the thyrotoxicosis and systemic lupus erythematosus-like symptoms coexisted and thereafter gradually declined in response to the decrease of titers of antithyroglobulin hemagglutination antibody and antimicrosomal hemagglutination antibody. To our knowledge, no such case has been previously reported. These observations strongly suggest that thyrotoxicosis in silent thyroiditis may be induced by an autoimmune mechanism.

Three patients who spontaneously developed persistent hypothyroidism during or following treatment with antithyroid drugs for Graves' hyperthyroidism.

Three patients with Graves' disease who spontaneously developed hypothyroidism after treatment with antithyroid drugs are described herein. Patient 1 developed a painful tender thyroid enlargement with a fever and accelerated erythrocyte sedimentation rate when she was receiving maintenance therapy with methimazole, and she progressed to persistent hypothyroidism with increased titers of antithyroglobulin and antimicrosomal antibodies and marked reduction of goiter size within the subsequent 2 months. Thyroid-stimulating hormone-binding inhibitory immunoglobulins (TBIIs) and thyroid stimulation-blocking antibody (TSBAb) were absent when she was hypothyroid. Hypothyroidism probably resulted from autoimmune thyroid destruction due to subacute aggravation of Hashimoto's thyroiditis. During the clinical course of patient 2, accelerated erythrocyte sedimentation rate and later transient increases of antimicrosomal and antithyroglobulin antibody titers were observed repeatedly (four times), and she finally fell into overt hypothyroidism. She also had negative results of tests for TBII and TSBAb. Her hypothyroidism appeared to result from repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis. Patient 3 fell into hypothyroidism when receiving a small dosage of methimazole. The TBII and TSBAb were strongly active when she developed hypothyroidism, which thus seemed to be due to blocking antibody. Patients with Graves' hyperthyroidism may eventually progress to hypothyroidism later by several different mechanisms. Severe and sudden or slowly repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis is one mechanism. Another may be the appearance of a blocking antibody to the TSH receptor.

The mechanism involved in the conversion of thyrotropin receptor-bound blocking-type immunoglobulin G (IgG) to the stimulating-type by anti-human IgG antibodies.

It has been reported that the addition of antibody (Ab) against human immunoglobulin G (IgG) converts TSH receptor-bound blocking-type IgG to stimulating-type IgG. However, the detail of converting mechanism remains unclear. In this study we examined the mechanism involved in this conversion using FRTL-5 cells. Blocking-type IgG was obtained from a patient with hypothyroidism. FRTL-5 cells were first incubated with IgG solution, then washed with PBS and exposed to antihuman IgG Ab. The effect of antihuman IgG Ab on converting activity was dose dependent. Maximal stimulation of cAMP was achieved with an antiserum dilution of 1:75. It seems likely that antimicrosomal Ab does not interfere with cAMP production, since IgG with a high anti-hemagglutination antibody titer did not show converting activity. Of the several kinds of antibodies tested, Ab against human IgG-Fab fragment was the most effective in converting ability, while the least effective were those against human IgG-Fc fragment. Although the divalent F(ab')2 fragment of antihuman IgG was significantly more effective in its converting ability than the monovalent Fab fragment, the Fab fragment itself also converted blocking IgG to the stimulating type in a dose-dependent manner. Accordingly, receptor cross-linking or aggregation does not play a major role in promoting this converting phenomenon. When cells were first exposed to blocking-type IgG and then to both antihuman IgG Ab and bovine TSH, cAMP production was much greater than the sum of each alone. However, anti-IgG Ab alone did not affect the binding of blocking-type IgG to receptor. These results suggest that the addition of antihuman IgG Ab not only converts blocking-type IgG to the stimulating type but also recovers TSH activity via a postreceptor step. Forskolin, like TSH, showed an additive effect on cAMP stimulatory action with antihuman IgG. In contrast, cholera toxin and antihuman IgG Ab were not additive. The reason for this discrepancy remains unknown. In summary, our observation indicates that 1) the converting phenomenon is induced via IgG-TSH receptor complexes; 2) the mechanism aside from receptor aggregation, i.e. the recognition of a critical domain in TSH receptor molecule, seems necessary for promoting converting phenomenon; and 3) the addition of antihuman IgG Ab affects a postreceptor step via TSH receptor structures that differ from the TSH-binding site.

Chronic thyroiditis with painful tender thyroid enlargement and transient thyrotoxicosis.

Clinical and laboratory findings and long term outcome (1.5-9 yr) in 7 women and 1 man with chronic thyroiditis (CT) who had painful tender thyroid enlargement were evaluated and compared with those in 11 women with subacute thyroiditis (SAT). Histological features consistent with SAT were not demonstrable, and various forms of CT (fibrous variant, diffuse, or focal lymphocytic thyroiditis) were observed. There were no differences in mean age, duration of symptoms, erythrocyte sedimentation rate, and C-reactive protein values in the 2 diseases. Seven patients had a history of goiter, and none had a history of a preceding upper respiratory tract infection. The mean white blood cell count was significantly lower in CT than in SAT patients. Six CT patients had transient thyrotoxicosis with a marked depression of radioactive iodine uptake. Mean serum T4 and T3 levels and T3 to T4 ratio in these 6 patients did not differ from those in the SAT patients. Five (all with high antimicrosomal antibody titers) of 8 CT patients developed persistent hypothyroidism. In contrast, none of the SAT patients became permanently hypothyroid. TSH binding inhibitory immunoglobulins and thyroid stimulation-blocking antibody at recent examination were negative in these 5 patients. Patients with this disorder present with transient thyrotoxicosis, with a marked depression of the thyroid radioactive iodine uptake, and often develop goitrous or atropic persistent hypothyroidism. This disorder may represent acute exacerbation of an underlying immunological process during the course of CT. To differentiate this syndrome from SAT, thyroid biopsy is necessary.

Lower serum free thyroxine (T4) levels in painless thyroiditis compared with Graves' disease despite similar serum total T4 levels.

Serum total T4 (T4), total T3 (T3), free T4 (FT4), free T3 (FT3), and T4-binding globulin concentrations and T3 resin uptake values were measured in 17 women with thyrotoxicosis due to painless thyroiditis (PT) and compared with the same parameters in 17 women with thyrotoxicosis due to Graves' disease (GD) with similar serum T4 levels. The mean serum T3 resin uptake value and T3, FT4, and FT3 concentrations in the PT patients were significantly lower than those in the GD patients. The mean serum T4-binding globulin concentration [20.2 +/- 4.2 (+/- SD) microgram/mL] in patients with PT did not differ significantly from those in patients with GD (18.0 +/- 2.6 micrograms/mL) and normal euthyroid women (21.9 +/- 4.0 micrograms/mL). The serum T3 to T4 (nanogram per microgram) ratio was higher than 20 in 14 GD patients, but lower than 20 in all patients with PT, whereas the individual serum FT3 to FT4 ratio values considerably overlapped in the 2 groups. In patients with PT, FT4 correlated well with T4 at various times during the clinical course. These findings indicate that the elevation in serum FT4 in patients with PT is mostly due to the increase in circulating T4 levels, whereas GD patients also have some diminution in T4 binding. The serum T3 to T4 ratio, but not the FT3 to FT4 ratio, may be helpful for differentiation between the two diseases.

A new type of familial central diabetes insipidus caused by a single base substitution in the neurophysin II coding region of the vasopressin gene.

We studied the genetic basis of familial neurohypophyseal diabetes insipidus in a Japanese family. The members had polyuria and a deficiency of plasma vasopressin (AVP). Polymerase chain reaction (PCR) amplified exons of the AVP-neurophysin-II gene were subcloned and sequenced. Exons 1 and 3 were normal, but nucleotide 1884 Guanine (G) in exon 2 was substituted with Thymine (T), which induced a substitution of glycine (Gly) for valine (Val). To examine the presence of this mutation in the affected subjects, we designed two mutated primers. One of them induced a new endonuclease restriction site in the PCR fragments from normal, and the other induced a new endonuclease restriction site from patients with the mutation. DNA fragments from two affected members of this family were amplified with this primer, and the PCR products were digested by endonuclease and resolved by electrophoresis. The results indicated that these subjects had both normal and mutant alleles, indicating that the mutation was heterozygous. We concluded that this mutation caused neurohypophyseal diabetes insipidus in this family.

Auditory brain stem responses in relation to the clinical symptoms of schizophrenia.

Auditory brain stem responses (ABSR) were examined systematically both in normal and schizophrenic subjects. All ABSR wave forms were evoked by click stimuli, which were delivered binaurally through headphones both to normal subjects and to a nondeteriorated group of schizophrenics. However, in the group of schizophrenics with marked deterioration of personality, not all wave forms were elicited, and the amplitudes were low. The characteristics of the ABSR wave forms correlated well with the clinical symptoms of the schizophrenic illness. The cause of these ABSR wave form changes in schizophrenics is discussed.

Descending projections from the gigantocellular tegmental field in the cat: cells of origin and their brainstem and spinal cord trajectories.

The trajectories and the cells of origin of the pontobulbar gigantocellular tegmental field descending pathways were studied in the cat using anterograde WGA-HRP and retrograde HRP techniques. Four main descending pathways and cells of origin were delineated: (1) Predominantly large neurons in the pontine gigantocellular tegmental field (average soma diameter = 43.4 microns) and rostral bulbar gigantocellular tegmental field (41.3 microns) gave rise to reticulospinal fibers descending in the ipsilateral medial longitudinal fasciculus and ventral funiculus and distributed in laminae V-X with an ipsilateral predominance. These were primarily large-diameter fibers. (2) Predominantly large neurons (46.9 microns) in the bulbar gigantocellular tegmental field gave rise to reticulospinal fibers descending in the contralateral medial longitudinal fasciculus and ventral funiculus. These were mainly large-diameter fibers. (3) Neurons of predominantly medium size (29.5 microns) in the pontine gigantocellular tegmental field gave rise to reticuloreticular fibers descending directly to and distributed bilaterally in the bulbar reticular formation. These were small-diameter fibers. (4) Neurons of predominantly medium size (28.9 microns) in the bulbar gigantocellular tegmental field gave rise to reticulospinal fibers descending in the ipsilateral reticular formation and lateral funiculus. These were small-diameter fibers.

Morphological and electrophysiological identification of gigantocellular tegmental field neurons with descending projections in the cat: II. Bulb.

There are three different descending projections from the bulbar gigantocellular tegmental field (BFTG) in the cat, as defined by intracellular recording and intracellular horseradish peroxidase (HRP) techniques. The first pathway arises from neurons which send axons to the contralateral medial longitudinal fasciculus (cMLF neurons); cMLF neurons show excitatory postsynaptic potentials (EPSPs) after stimulation of the ipsilateral pontine gigantocellular tegmental field (PFTG). Most cMLF neurons have large ellipsoid-polygonal somata (mean, 56.8 micron), thick axons (average diameter, 3.09 microns), mostly non-spiny dendrites and dendritic fields flattened in the anteroposterior direction. No cMLF neurons with axon collaterals in the BFTG are present in the data of this study. The second pathway arises from neurons which send axons to the ipsilateral MLF (iMLF neurons); iMLF neurons show EPSPs after stimulation of the ipsilateral PFTG. Most iMLF neurons have large ellipsoid-polygonal somata (mean, 60.2 microns), thick axons (average diameter, 3.00 microns), mostly non-spiny dendrites and dendritic fields that are only slightly flattened in the anteroposterior direction. As with cMLF neurons, no iMLF neurons with axon collaterals in the BFTG are present in the data of this study. The third pathway arises from neurons that send axons directly into the ipsilateral caudal bulbar reticular formation (iBRF neurons). Most iBRF neurons have smaller ellipsoid-polygonal somata (mean, 38.6 microns), thinner axons (average diameter, 1.84 microns), mostly nonspiny dendrites, and dendritic fields that are flattened in the anteroposterior direction. In contrast to cMLF and iMLF neurons, axon collaterals are present in 73% of iBRF neurons. About half of iBRF neurons have bifurcated axon collaterals with both anterior and posterior projections, and in these neurons antidromic spike potentials are elicited by stimulation of the ipsilateral PFTG.

Morphological and electrophysiological identification of gigantocellular tegmental field neurons with descending projections in the cat: I. Pons.

Two different descending projections from the pontine gigantocellular tegmental field (PFTG) were defined by the use of intracellular recording and intracellular horseradish peroxidase (HRP) techniques in the cat. Type I neurons (reticulospinal neurons) had antidromic spike potentials produced by stimulation of the ipsilateral medial longitudinal fasciculus (MLF) and sent axons to the ipsilateral MLF. Most type I neurons had large ellipsoidpolygonal somata (mean, 59.7 microns), thick axons (average diameter, 3.33 microns), and slightly oblate large dendritic fields. The mean anteroposterior extent of the dendritic field was 1,492 microns, the mean mediolateral extent was 1,784 microns, and the mean dorsoventral extent was 1,562 microns. There were no type I neurons with axon collaterals. In contrast, type II neurons (reticuloreticular neurons) had antidromic spike potentials produced by stimulation of the bulbar reticular formation (BRF) and sent axons directly to the BRF. In comparison with type I neurons, most type II neurons had smaller ellipsoidpolygonal somata (mean, 40.2 microns), thinner axons (average diameter, 2.32 microns), and smaller, slightly oblate dendritic fields. The mean anteroposterior extent of the dendritic field was 1,264 microns; the mean mediolateral extent was 1,511 microns; and the mean dorsoventral extent was 1,226 microns. Also in contrast to type I neurons, 36% of type II neurons had axon collaterals.