Statistical analysis of clinical, radiographic, and histologic features of temporomandibular arthropathy

For a variety of reasons, the past few years have brought about a tremendous emphasis on conditions affecting the temporomandibular joint and associated structures. Although important advances are being made relative to the diagnosis and treatment of these conditions, a myriad of problems remain for the practitioner who tries to sort through the literature or who attends courses in order to determine a means for properly diagnosing and treating these patients. This article attempts to develop correlations between certain clinical and radiographic findings documented by histologic evaluation as a beginning guide to more sound diagnosis.     

A surgically recovered case of spontaneous rupture of the esophagus--the significance of preoperative esophagoscopy for direct suture

A 65-year-old man with spontaneous rupture of the esophagus survived with a direct suture of the esophagus 15 hours after the onset of symptoms. Endoscopic examination of the esophagus was especially of great help in determining the surgical procedure in this patient, and we want to stress the importance of prompt diagnosis and immediate surgery for this disease.     

Comparison of PET, MRI, and CT with pathology in a proven case of Alzheimer's disease

Positron emission tomography (PET) with fluorodeoxyglucose (FDG), magnetic resonance imaging (MRI), and CT were carried out in a patient with Alzheimer's disease 16 months before he died. At autopsy, the gross appearance of the brain correlated with MRI and CT, which showed some regional atrophy. These were much less revealing than PET, which correlated with microscopic findings of neuronal loss and proliferation of glia. In areas of moderately impaired local cerebral metabolic rate of glucose, as revealed by reduced FDG uptake, there was some gliosis, primarily around the numerous senile plaques. In areas of severe metabolic impairment, there was a profound loss of neurons, extensive gliosis, and a diminished appearance of plaques. PET-FDG is a better measure of the severity of Alzheimer's disease than MRI or CT, because it reflects the degree of neuronal pathology.     

gamma-Aminobutyric acid (GABA) causes consistent depolarization of neurons in the guinea pig supraoptic nucleus due to an absence of GABAB recognition sites

The action of gamma-aminobutyric acid (GABA) in the supraoptic nucleus was investigated using guinea pig brain slices. GABA produced a membrane depolarization accompanied by a decrease in the input resistance. The action of GABA was concentration-dependent throughout a wide range of concentrations (10(-7)-10(-3) M). In none of the cells examined, a membrane hyperpolarization was observed. The reversal potential for the depolarization induced by GABA was about 25 mV positive to the resting membrane potential. The amplitude of the GABA-induced depolarization was increased to 1.5 X the control by reducing the external Cl- from 134.2 mM to 10.2 mM. The action of GABA was readily antagonized by relatively low concentrations of bicuculline (10(-5) M). The action of GABA in the hippocampus or in the anterior hypothalamus was markedly different from that in the supraoptic nucleus, i.e. GABA produced both depolarizing and hyperpolarizing responses in the hippocampus and consistently a hyperpolarization in the anterior hypothalamus. The depolarizing but not the hyperpolarizing response in the hippocampus was selectively blocked by picrotoxin (2 X 10(-5) M) or by bicuculline (10(-5) M). The depolarizing component was dependent on the external Cl- concentration and had a reversal potential similar to that of the depolarization induced by GABA in the supraoptic nucleus. The hyperpolarizing component was resistant to bicuculline and had a reversal potential about 30 mV negative to the resting membrane potential.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of dexamethasone on central and peripheral ACTH systems in the rat

To investigate the simultaneous effects of dexamethasone on peripheral and central adrenocorticotropic hormone (ACTH) systems, rats were treated with dexamethasone or saline for 4 days. Pituitary, plasma, hypothalamus and cerebrospinal fluid (CSF) were then collected and analyzed for ACTH immunoreactivity. Additionally, hypothalamic tissue extracts were analyzed for corticotropin-releasing hormone (CRH) immunoreactivity. Dexamethasone significantly lowered peripheral levels of ACTH as measured in pituitary and plasma. Hypothalamic ACTH content significantly increased while CSF ACTH significantly decreased with dexamethasone treatment. Hypothalamic CRH concentrations showed a small but statistically insignificant decrease. These results suggest that prolonged exposure to dexamethasone affects central as well as peripheral ACTH activity, corroborate our previous findings in rhesus monkeys of decreased CSF ACTH in response to prolonged dexamethasone treatment, suggest that dexamethasone may inhibit the release of ACTH from hypothalamic neurons into the CSF, and provide evidence that the effect of dexamethasone on pituitary ACTH content is of greater magnitude than its effect on hypothalamic CRH.     

Evidence for dual modulation of pepsinogen secretion using isoproterenol, carbachol, CCK-8, forskolin, 8 bromo-cAMP, and A23187 probes

The cellular mechanisms by which pepsinogen (PNG) secretion is controlled are not understood. The aim of this study was to explore whether modulation of PNG secretion is mediated by cAMP or calcium-calmodulin (C-C). PNG secretion in isolated rabbit gastric fundic glands (IGG) was tested, using agents believed to act via cAMP or C-C. IGG were stimulated for 30 minutes with histamine (H) 10(-5) M, isoproterenol (I) 10(-5) M, carbachol (C) 10(-5) M, cholecystokinin-octapeptide (CCK-8) 10(-7) M, forskolin (F) 10(-5) M, 8 bromo-cAMP (8B) 10(-3) M, and A23187 (A) 10(-6) M. PNG levels were determined by spectrophotometric assay of hemoglobin digestion products. PNG amounts secreted were (mean per cent above basal levels of total IGG PNG units +/- SEM): H, -0.02 +/- 0.30%; I, 3.5 +/- 0.9%; C, 5.1 +/- 2.2%; CCK-8, 5.3 +/- 1.5%; F, 10.6 +/- 3.8%; 8B, 13.8 +/- 4.5%; A, 2.1 +/- 1.1%. All secretagogues except H stimulated PNG release significantly above basal levels (p less than 0.05). A primary histaminergic mechanism for pepsinogen secretion is unlikely. Since two other adenylate cyclase activators, isoproterenol and forskolin and the 3':5'-cyclic adenosine monophosphate analog 8-bromo cAMP stimulated pepsinogen secretion, cAMP-dependence is probable. Since carbachol, CCK-8, and A23187, which are believed to act via calcium-calmodulin, also stimulated pepsinogen secretion, this system, too, presumably plays a substantial role. Thus the data support a dual 3':5'-cyclic adenosine monophosphate/calcium-calmodulin modulation of pepsinogen secretion.     

Neutropenic enterocolitis in adults with acute leukemia

Neutropenic enterocolitis has been previously described only by case reports and literature reviews. Of 499 adults with acute leukemia seen over a 23-year period (1962 to 1985), 13 cases (2.6%) of neutropenic enterocolitis have been reported. Eleven of these 13 patients were profoundly neutropenic (mean white blood cell count, 472/cu mm) and developed abdominal symptoms during either initial induction or relapse of acute leukemia. Histologic confirmation was available in ten cases, five cases after surgical resection and five cases at autopsy after nonoperative management. Three patients with isolated ileocecal inflammation without infarction at the time of surgery were successfully managed without resection. Five patients treated with surgery died four to 64 weeks postoperatively (mean survival, 21.6 weeks) of nonsurgical complications of leukemia. Three patients were still alive, one patient 42 months after right hemicolectomy and two patients five months after exploration only. All five patients managed medically died an average of 1.4 days (range, zero to four days) after the onset of abdominal pain. Survival in patients with acute leukemia who develop neutropenic enterocolitis is determined by early recognition and appropriate surgical exploration that can be expected to yield an acceptable operative mortality.     

Effect of temperature on blood flow and metabolism in a neurovascular island skin flap

Using the buttock flap in 29 white Yorkshire pigs, blood flow and O2 consumption were measured at dermal temperatures between 35 degrees C and 15 degrees C. Flow was measured with an electromagnetic flowmeter and O2 consumption was calculated as the product of blood flow and the difference in flap A-VO2. Baseline flow was 6.6 +/- .9 (SE) ml/100 g/min at 35 degrees C and 3.1 +/- .02 (SE) ml/10 g/min at 15 degrees C. Blood flow through the flap stopped completely at a dermal temperature of 14 degrees C. Oxygen consumption was 0.16 +/- .02 (SE) ml/100 g/min at 35 degrees C and 0.04 +/- 0.01 (SE) ml/100 g/min at 15 degrees C. At 20 degrees C blood flow was 4.3 ml/100 g/min and metabolism was .04 ml/100 g/min. In other words, blood flow was 65% of baseline, while O2 consumption was only 25% of baseline. The therapeutic effect of local cooling at 20 degrees C deserves further investigation. The cessation of flow at 14 degrees C may be caused by increased plasma viscosity.     

Role of blood flow in acute gastric lesion after hepatectomy and effect of prostaglandin I2 and H2-receptor antagonist

In order to investigate the cause of gastric mucosal lesion following hepatectomy, changes of gastric, pancreatic and femoral arterial blood flow were measured in 70% hepatectomized rabbits. Following administration of 0.5 microgram/kg of GRP, gastric blood flow increased to 120% of the basal level in the controls, but reached to only 107% of the basal level in the hepatectomized rabbits. Following hemorrhage of 10% of the total blood volume seven days after hepatectomy, blood flow decreased to 55% of the basal level in the stomach, 57% in the pancreas and 76% in the femoral artery. Although pancreatic blood flow recovered to 81% of the basal level, gastric blood flow remained low, 59% of the basal level, suggesting poor recovery of gastric blood flow as compared to pancreatic blood flow. Administration of PGI2 and ranitidine in hepatectomized rabbits with hemorrhage conferred a considerable degree of recovery of gastric blood flow in the PGI2 group (from 56% to 80%) and in the ranitidine group (from 52% to 72%). Thus, disturbance of reaction and poor recovery of gastric blood flow following hemorrhage were indicated as important causes of acute gastric mucosal lesion associated with hepatectomy. Both PGI2 and ranitidine appeared to be effective for the maintenance of gastric blood flow after hepatectomy.