Intellectual functioning and the long-term course of schizophrenia-spectrum illness.

BACKGROUND: Recent neurodevelopmental models of schizophrenia, together with substantial evidence of neurocognitive dysfunction among people with schizophrenia, have led to a widespread view that general cognitive deficits are a central aspect of schizophrenic pathology. However, the temporal relationships between intellectual functioning and schizophrenia-spectrum illness remain unclear. METHOD: Longitudinal data from the Copenhagen High-Risk Project (CHRP) were used to evaluate the importance of intellectual functioning in the prediction of diagnostic and functional outcomes associated with the schizophrenia spectrum. The effect of spectrum illness on intellectual and educational performance was also evaluated. The sample consisted of 311 Danish participants: 99 at low risk, 155 at high risk, and 57 at super-high risk for schizophrenia. Participants were given intellectual [Weschler's Intelligence Scale for Children (WISC)/Weschler's Adult Intelligence Scale (WAIS)] assessments at mean ages of 15 and 24 years, and diagnostic and functional assessments at mean ages 24 and 42 years. RESULTS: Intellectual functioning was found to have no predictive relationship to later psychosis or spectrum personality, and minimal to no direct relationship to later measures of work/independent living, psychiatric treatment, and overall severity. No decline in intellectual functioning was associated with either psychosis or spectrum personality. CONCLUSIONS: These largely negative findings are discussed in the light of strong predictive relationships existing between genetic risk, diagnosis and functional outcomes. The pattern of predictive relationships suggests that overall cognitive functioning may play less of a role in schizophrenia-spectrum pathology than is widely believed, at least among populations with an evident family history of schizophrenia.

Distribution of intestine-associated lymphoid tissue, aberrant crypt foci, and tumors in the large bowel of 1,2-dimethylhydrazine-treated mice.

Six-week-old male CF-1 mice were fed the AIN-76 diet, given eight weekly s.c. injections of either the colon carcinogen 1,2-dimethylhydrazine or saline, and killed 24 weeks after the last injection. Parameters measured in the large bowel included the incidence and locations of all intestine (gut)-associated lymphoid tissue (GALT) sites; the locations, incidence, and sizes of all aberrant crypt foci (ACF); and the incidence, locations, and types of all overt tumors. In saline-treated mice the distribution of GALT along the length of the large bowel was bimodal, with a majority peak of lymphoid nodules occurring in the distal large bowel and a minority peak occurring in the proximal large bowel. No ACF or tumors were present in the large bowel of the saline-treated mice. In 1,2-dimethylhydrazine-treated mice the majority of ACF were present in the middle third of the colon, between the two peaks of GALT, but the majority of the tumors were found over the GALT in the distal colon. There was a significant positive linear regression relationship between the numerical distribution of GALT and the numerical distribution of tumors along the length of the large bowel. There was no significant relationship between the distribution of ACF and the distribution of (a) tumors or (b) GALT along the length of the large bowel. Thus the numerical density of lymphoid nodules, not the numbers or distribution of ACF, was the significant predictor of the distribution of tumors in the large bowel of 1,2-dimethylhydrazine-treated mice. It is proposed that lymphoid nodules in the distal large bowel play a promotional role following initiation of colon carcinogenesis and that ACF have little if any malignant potential in the mouse.

Dietary fibre on cell proliferation in large bowel mucosal crypts near or away from lymphoid nodules and on mineral bioavailability.

The effect of consumption for 24 weeks of different amounts (0%, 5% or 10% w/w) of fermentable (pectin and guar gum) or nonfermentable (cellulose and lignin) dietary fibres on cell proliferation and other parameters in large bowel mucosal crypts was studied in rats. In all 12 dietary groups, the crypts located over the distal aggregate of lymphoid nodules (ALN) had more colchicine arrested metaphase figures per midaxial crypt section (MC) and a longer crypt column height than crypts located three to four cm away from this ALN. These differences are attributed to the tropic influence of nodular cells in the ALN. Consumption of fermentable fibre decreased pH in the lumen of the caecum, and glucose, Zn and Cu in serum but increased Ca and Mg in serum. The decrease in caecal pH and serum glucose was significantly correlated with a decrease in MC. Increased intake of the nonfermentable fibre types increased faecal bulk but had no significant correlation with the other measured crypt parameters. Multiple regression analyses was used to model the relationships between the mucosal crypt criterion variables and the two measured predictor variables, caecal pH and serum glucose. Relationships between dietary fibre, ALN, MC, bioavailability of dietary minerals and risk of colorectal cancer are discussed.

Infectious mononucleosis in the older patient.

Six cases of infectious mononucleosis in patients more than 60 years old were reviewed. The geriatric patient with infectious mononucleosis often presents with nonspecific constitutional symptoms, without exudative pharyngitis. The disease may present as fever of obscure origin or mimic chronic lymphocytic leukemia in this age group. Diagnosis is established through characteristic findings on hematologic and serologic studies.

Canal geometry changes associated with axial compressive cervical spine fracture.

STUDY DESIGN: A laboratory study using isolated ligamentous human cadaveric cervical spines to investigate canal occlusion during (transient) and after (steady-state) axial compressive fracture. OBJECTIVES: To determine whether differences exist between transient and postinjury canal occlusion under axial compressive loading, and to examine the effect of loading rate on canal occlusion. SUMMARY OF BACKGROUND DATA: Prior studies have shown no correlation between neurologic deficit and canal occlusion measurements made on radiographs and computed tomography scans. The authors hypothesized that postinjury radiographic assessment does not provide an appreciation for the transient occlusion that occurs during the traumatic fracture event, which may significantly affect the neurologic outcome. METHODS: Twelve human cervical spines were instrumented with a specially designed canal occlusion transducer, which dynamically monitored canal occlusion during axial compressive impact. Six specimens were subjected to a fast-loading rate (time to peak load, approximately 20 msec), and the other six were subjected to a slow-loading rate (time to peak load, approximately 250 msec). After impact, two different postinjury canal occlusion measurements were performed. RESULTS: Each of the six specimens subjected to the fast-loading rate incurred burst fractures, whereas the slow-loading rate produced six wedge-compression fractures. For the fast-rate group, the postinjury occlusion-measurements were significantly smaller than the transient occlusion. In contrast, transient occlusion was not found to be significantly different from postinjury occlusion in the slow-rate group. All of the comparisons between loading rate groups showed significant differences, with the fast-rate fractures producing larger amounts of canal occlusion in every category. CONCLUSIONS: The findings indicate that even if canal occlusion could be measured immediately after axial compressive trauma, the measurement would underestimate the maximal amount of transient canal occlusion. Therefore, postinjury measurement of canal occlusion may indicate a smaller degree of neurologic deficit than what might be expected if the transient occlusion could be measured.

The effect of post-injury spinal position on canal occlusion in a cervical spine burst fracture model.

STUDY DESIGN: The canal space of burst-fractured, human cervical spine specimens was monitored to determine the extent to which spinal position affected post-injury occlusion. OBJECTIVE: To test the null hypothesis that there is no difference in spinal canal occlusion as a function of spinal positioning for a burst-fractured cervical spine model. SUMMARY OF BACKGROUND DATA: Although previous studies have documented the effect of spinal positioning on canal geometry in intact cadaver spines, to the authors' knowledge, none has examined this relationship specifically in a burst fracture model. METHODS: Eight human cervical spine specimens (levels C1 to T3) were fractured by axial impact, and the resulting burst injuries were documented using post-injury radiographs and computed tomography scans. Canal occlusion was measured using a custom transducer in which water was circulated through a section of flexible tygon tubing that was passed through the spinal canal. Any impingement on the tubing produced a rise in fluid pressure that was monitored with a pressure transducer. Each spine was positioned in flexion, extension, lateral (and off-axis) bending, axial rotation, traction, and compression, while canal occlusion and angular position were monitored. Occlusion values for each position were compared with measurements taken with the spine in neutral position. RESULTS: Compared with neutral position, compression, extension, and extension combined with lateral bending significantly increased canal occlusion, whereas flexion decreased the extent of occlusion. In extension, the observed mechanism of occlusion was ligamentum flavum bulge caused by ligament laxity resulting from reduced vertebral body height. CONCLUSIONS: Increased compression of the spinal cord after injury may lead to more extensive neurologic loss. This study demonstrated that placing a burst-fractured cervical spine into either extension or compression significantly increased canal occlusion as compared with occlusion in a neutral position.

Lymphoma presenting as a Sister Mary Joseph's nodule.

Metastatic tumors to the umbilicus, often referred to as Sister Mary Joseph's nodules, are rare. In general, they have been described in association with intra-abdominal malignancy, especially adenocarcinomas, although there has been one case report of malignant myeloma spreading to the umbilicus. Lymphomas, however, historically seem to reject the umbilicus as a site of metastatic spread. The following case report is, to our knowledge, the first reported instance of lymphoma presenting as an umbilical nodule.

Choledochoduodenostomy. A safe and efficacious alternative in the treatment of biliary tract disease.

A review of 75 patients who underwent side-to-side choledochoduodenostomy as primary or secondary treatment for various forms of biliary tract disease was performed. Ages of patients ranged from 23 to 89 years (mean of 61 years), with 40 per cent of patients 70 years or older. All anastomoses were created with a minimal diameter of 2 cm. During a follow-up period ranging from 6 months to 8 years, there was no incidence of ascending cholangitis or anastomotic stricture. Six patients continued to have non-specific complaints of abdominal pain postoperatively that could not be attributed to the "sump syndrome" after necessary diagnostic studies were performed. The overall morbidity and mortality was 6.6 per cent and 1.3 per cent, respectively. This study confirms the notion that choledochoduodenostomy can be performed safely, with good results, particularly in the expanding high-risk elderly patient population.

Shipboard medicine on package cruises.

Cheap package cruises have become very popular in Great Britain, but the ships used for these cruises are often not suitable for elderly, handicapped, and mentally unfit people. The cruises run to very tight schedules with many strenuous shore excursions, and do not necessarily constitute restful holidays at sea. Many passengers who embark on these cruises are suffering from pre-existing diseases, which may become exacerbated during the voyage. Such patients should be forewarned and should be equipped by their doctors with a covering letter giving full details of their medical condition and its treatment.

Diaphragmatic trauma in southern Saskatchewan--an 11-year review.

An 11-year retrospective review of 51 patients with diaphragmatic injuries revealed 33 blunt and 18 penetrating injuries. In the blunt trauma group 24 were left-sided and nine were on the right side. Preoperative diagnosis was made in 24 patients. Delayed diagnosis (greater than 24 hours) during life occurred in four patients and two injuries were found at autopsy. Chest X-ray was diagnostic or highly suggestive in 23 patients. All patients in this group had associated extra-abdominal injuries; 23 patients had concomitant intraabdominal injuries. Transabdominal repair was performed in 24 patients. Four deaths occurred in the blunt injury group. The penetrating diaphragmatic wounds consisted of 14 left-sided, three right-sided, and one pericardial wound. Preoperative diagnosis occurred in only three patients. The penetrating wound, hypotension, or peritoneal signs dictated operation in the remaining 15 patients. One death occurred from peritonitis and septic shock. Blunt and penetrating diaphragmatic injuries remain a diagnostic challenge and associated injuries determine the outcome.

Acutely administered polychlorinated biphenyls (PCBs) decrease splenic cellularity but increase its ability to cause graft-versus-host reactions in BALB/c mice.

A single intraperitoneal injection of 1000 mg/kg body weight of a PCB mixture (Aroclor 1242) to adult male BALB/cc mice caused not only a relative spleen enlargement, but also an absolute spleen lymphocyte depletion. However, there was an enrichment of spleen T cells necessary to cause a graft-versus-host reaction (GVHR) in (C3H x BALB/c) F1 neonates. The effect was present 6 days after PCB administration and was no longer present on days 12-13. These studies suggest a transient effect of acutely administered PCBs on splenic lymphocytes (B cells, null cells, some T cells) other than mature GVH inducing T cells. The effect may be either similar to or possibly indirectly mediated by corticosteroids.

The responses of plasma biochemical parameters to a 56-km race in novice and experienced ultra-marathon runners.

A number of blood biochemical parameters, including the activities of the plasma enzymes creatine kinase (CK), aspartate aminotransferase (ASAT), lactate dehydrogenase and alkaline phosphatase, were measured in 23 athletes before, and immediately after a 56-km running race. Of the 23 athletes, 18 had previously completed standard 42-km marathon or longer (up to 90-km) ultra-marathon races, whereas not one of the other five athletes had previously run in a long-distance race. After the race, plasma CK and ASAT activities had both risen at least 280% more in the novice runners despite their much slower mean running speed (9.8 +/- 0.4 vs. 13.8 +/- 0.3 hm/h). There were no other inter-group differences in the absolute levels of the other measured biochemical parameters, although the rise in plasma calcium during the race was significantly greater in the experienced marathon runners. This study shows that either higher levels of training, or previous ultra-marathon racing experience, or both, is associated with lower immediate post-exercise levels of plasma enzyme activity. This is compatible with the finding that physical training reduces post-exercise plasma enzyme levels.

Biochemical parameters in athletes before and after having run 160 kilometres.

A number of biochemical and haematological parameters, including plasma electrolytes, parameters of hepatic and renal function, plasma enzymes and free fatty acids were measured in 13 athletes before and after a 160-km 24-hour race. The runners were divided into 2 groups: group A, who competed the 160 km within 24 hours and group B, who either ran for 24 hours, or who retired before completing the distance. Minimal changes were found in the plasma electrolyte patterns in either group, whereas blood urea and creatinine levels increased during the race. The plasma enzymes increased to varying extents, the greatest increases being in lactic dehydrogenase, aspartate aminotransferase and the skeletal muscle specific MM isoenzyme of creatinine phosphokinase. Total bilirubin also increased, but no conclusive evidence of hepatic decompensation was found. Plasma free fatty acids levels were very markedly raised in 12 of the runners, the highest increases occurring in group A. All runners ingested carbohydrate during the race and this probably explains why the blood glucose levels increased slightly but remained within normal limits in all the athletes at the end of the race.

Zinc deprivation promotes progression of 1,2-dimethylhydrazine-induced colon tumors but reduces malignant invasion in mice.

The aim of this study was to characterize colon tumor development and invasiveness associated with dietary zinc deprivation. Colon carcinogenesis was initiated by eight weekly subcutaneous injections of 1,2-dimethylhydrazine (DMH) at 12 mg DMH base/kg body wt in groups of mice maintained on diets containing 30 micrograms/kg dietary zinc (zinc adequate, ZA) or 3 micrograms/kg dietary zinc (zinc deprived, ZD). All mice were killed 24 weeks after the last injection of DMH. Mean zinc concentration in the liver was significantly lower in the ZD group than in the ZA group. The total number of grossly detectable colon tumors was the same in both dietary groups. However, histopathological study of each tumor revealed significantly more adenomatous polyps (AP) and invasive adenocarcinomas (CA) in the ZA group, whereas the ZD group had significantly more noninvasive carcinomas in situ (CIS). It appears that zinc deprivation stimulated progression of AP to noninvasive CIS but retarded the progression of noninvasive CIS to invasive CA. Immunohistochemistry of tumors from ZA and ZD mice indicated increased amounts of type IV collagenase in epithelial tumor cells and in stromal cells adjacent to tumor tissue regardless of the amount of dietary zinc consumed. It is suggested that zinc deprivation may limit function of zinc-requiring enzymes such as superoxide dismutase and type IV collagenase, resulting in enhanced progression of AP to noninvasive CIS and retardation of invasion of CIS to become CA, respectively.

MMPI variables predictive of schizophrenia in the Copenhagen High-Risk Project: a 25-year follow-up.

Moldin et al. (1) have identified a cluster of Minnesota Multiphasic Personality Inventory (MMPI) scales that discriminate adolescents at risk for schizophrenia from those not at risk. The present study examines how well Moldin's scales predict schizophrenic decompensation in a sample of 207 Danish adolescents at high genetic risk for schizophrenia. Subjects were assessed using a modified, 304-item MMPI in 1962 (mean age= 15.1 years) and diagnosed in 10-year and 25-year follow-ups. Premorbidly, schizophrenic subjects (n=31) scored higher than subjects with no mental illness on the frequency (F) and psychoticism (PSY) scales. When paranoid and non-paranoid preschizophrenics were separated, three scales (F, Pz (paranoid schizophrenia) and PSY) significantly discriminated paranoid preschizophrenics. Discriminant function analyses confirmed these results. It is concluded that the MMPI may be useful for identifying schizophrenia premorbidly.

The effect of exercise on bleeding time and local production of prostacyclin and thromboxane.

Exercise at a heart rate corresponding to 30% VO2max for 15 min was associated with an increase in the volume of bleeding time blood from a mean of 133 microliters before exercise to a mean of 218 microliters during and immediately after the exercise. There was similarly an increase in thromboxane B2 production from 6.40 nmol.l-1 before to 11.50 nmol.l-1. Most subjects also showed an increase in the length of the bleeding time and in the production of bleeding time 6-keto-PGF1 alpha. The extent of increase in the bleeding time and in production of 6-keto-PGF1 alpha was quite variable, with subjects showing the largest increases in bleeding time also demonstrating the greatest increases in 6-keto-PGF1 alpha (r = 0.76, P = 0.004). The ingestion of aspirin before exercise markedly inhibited basal bleeding time thromboxane B2 production and blocked the exercise-associated increments in thromboxane B2 and 6-keto-PGF1 alpha production. While the aspirin itself increased the length of the bleeding time, there was not any further increase associated with exercise. In contrast to the effects of acute short-term exercise, long-distance running was associated with a significant decrease in bleeding time, but no change in bleeding time blood volume, bleeding time thromboxane B2, or bleeding time 6-keto-PGF1 alpha. The results show that acute low-level exercise can be associated with significant changes in the volume of blood oozing from a bleeding time incision and in the amount of thromboxane production stimulated at the incisional site. Following exhaustive exercise of long duration, the above changes are no longer seen.