In the last few years, there has been a growing interest in exploring the association between risk factors such as overweight, obesity and physical activity, and incidence of various cancers.Meta-analysis was performed to investigate the risk ratio of follicular lymphoma incidence and mortality in overweight and obese individuals, and in individuals with a different physical activity levels using the random-effects model.A literature search through September 2016 was performed.Case-control studies accounted for over 2.100 cases and 12.700 controls, whereas cohort studies accounted for over 2.600 cases in cohort of about 3.000.000individuals.In overweight individuals (body mass index between 25 and 29.99 kg/m 2 ) risk ratio for the development of follicular lymphoma was 1.03 (0.95-1.11; 95% CI; p = 0.51) and in obese (body mass index ≥ 30 kg/m 2 ) it was 1.15 (1.01-1.31;95% CI; p = 0.04) when compared to individuals with normal body mass index (< 25 kg/m 2 ).The risk ratio of specific follicular lymphoma mortality in overweight was 0.59 (0.38-0.91; 95% CI; p = 0.02), while in obese patients it was 1.08 (0.68-1.71; 95% CI; p = 0.75).In patients with the highest physical activity levels, the risk ratio for follicular lymphoma occurrence was 0.95 (0.75-1.21; 95% CI; p = 0.68) when compared to patients that had the lowest physical activity levels.In summary, our meta-analysis has shown statistically significant direct association between obesity and follicular lymphoma incidence.
Pancreatic tissues from 22 patients with a wide variety of types of shock were obtained within minutes of somatic death for light and electron microscopy and for cytochemical studies. By light microscopy, it was difficult to ascertain any differences between the shock groups; however, electron microscopy disclosed subcellular alterations that could be correlated well with the type, severity, and duration of shock. Mild cases of shock or shock of short duration showed mild cell damage, while extreme cases of hemorrhagic or septic shock showed cell death and necrosis. No morphological evidence for lysosomal initiation of damage was seen, but it is clear that the pancreas can undergo severe cell injury during shock that could result in release of further damaging enzymes, most probably from zymogen granules rather than from lysosomes.
Thirty cases of islet cell carcinoma of the pancreas diagnosed at Memorial Hospital were studied. There were 17 male and 13 female patients. The average age was 44 years. Most of the tumors were located in the body or tail of pancreas; in 25 instances, the primary tumor was larger than 6 cm. Epigastric pain, hypoglycemia, and jaundice were frequent primary clinical presentations. No morphological differences were found between functioning and nonfunctioning tumors. Size of tumor, local tissue infiltration, and vascular invasion were helpful; but they were not absolute parameters aiding in the differentiation of benign and malignant tumors. Twenty-six patients had metastatic disease at time of diagnosis. Liver, regional lymph nodes, bones, and peritoneum were common sites of metastases. The average survival was 3.9 years. The cumulative five-year survival rate was 65%.
Recent investigations in systemic lupus erythematosus (SLE) have disclosed the presence of paramyxo-virus-like nucleocapsids in the cytoplasm of renal endothelial cells of patients with this disease. Elaborate techniques have failed to demonstrate conclusively that these are indeed viruses. Concomitantly, there is increasing evidence that SLE patients have defective cell-mediated-immunity. A 3-year-old child with SLE exhibited clinical evidence of defective cellular immunity. At postmortem, paramyxoviruslike tubular structures were demonstrated in her kidneys. Additional findings included the presence of intracytoplasmic viral particles consistent morphologically with herpes simplex virus in neurons from the lateral geniculate body and numerous "nuclear bodies" in neurons and glial cells. A dysplastic thymus gland demonstrated virtual absence of lymphocytes and was devoid of Hassall corpuscles, unlike the thymus usually seen in SLE.
Recent investigations in systemic lupus erythematosus (SLE) have disclosed the presence of paramyxo-virus-like nucleocapsids in the cytoplasm of renal endothelial cells of patients with this disease. Elaborate techniques have failed to demonstrate conclusively that these are indeed viruses. Concomitantly, there is increasing evidence that SLE patients have defective cell-mediated-immunity. A 3-year-old child with SLE exhibited clinical evidence of defective cellular immunity. At postmortem, paramyxoviruslike tubular structures were demonstrated in her kidneys. Additional findings included the presence of intracytoplasmic viral particles consistent morphologically with herpes simplex virus in neurons from the lateral geniculate body and numerous "nuclear bodies" in neurons and glial cells. A dysplastic thymus gland demonstrated virtual absence of lymphocytes and was devoid of Hassall corpuscles, unlike the thymus usually seen in SLE.
Administration of D-serine to rats induced acute necrosis of the proximal straight tubules, proteinuria, glucosuria, and aminoaciduria. Proteinuria and glucosuria developed at the onset of tubular necrosis and disappeared when the tubules were completely relined by new epithelium. Our findings suggest (1) that abnormal loss of protein and glucose in urine is due to diffusion of these substances from interstitium to tubular fluid across the denuded permeable basement membranes of the necrotic tubules, and (2) that tubular cells normally are a barrier to diffusion of certain solutes betweeen interstitial and tubular fluids. Amino-aciduria preceded the onset of tubular necrosis and increased excretion of some amino acids persisted after tubular repair. Thus, D-serine-induced aminoaciduria may be due to impaired reabsorption of amino acids by the injured proximal straight tubules, as well as by backward diffusion of amino acids from the interstitium.
Rats were infused for three hours with doses of calcium gluconate to elevate serum calcium level and were killed either immediately after infusion or after 24 hours. Necrosis of proximal tubular cells was observed when serum calcium level was 16.0 mg/dl or higher. Above 16.0 mg/dl, an additional 5% of renal tubular profiles contained damaged cells for each 1 mg/dl in serum calcium. No difference in extent of damage was found in rats killed immediately or after 24 hours. Initial changes were formation of granular dense bodies in mitochondria, cell swelling, rupture, and extensive mitochondrial calcification. Renal tubular basement membrane changes appeared to be initiated by protrusion of cytoplasmic buds, forming ovoid bodies, which became embedded in the basement membrane. These ovoid bodies then appeared to serve as a nidus for further extensive basement membrane calcification.
Thioflavin S (TS), a fluorescent dye, was used to visualize the distribution of coronary flow within the area of ischemia produced by circumflex artery occlusions. In the ischemic region, TS failed to penetrate the subendocardium and was seen in the subepicardium. Even though collateral flow was noted in the subepicardium, studies with methylene blue showed that it was inadequate to prevent the development of ischemia. The proportion of the posterior papillary muscle and subjacent myocardium showing TS nonfluorescence was similar after 15 and 60 minutes of ischemia and correlated with maximum lead II ST segment elevation and the percent of grossly injured myocardium found at 60 minutes postocclusion. The results suggest that flow to ischemic myocardium is reduced to the greatest extent in the subendocardium, ie, the site where irreversible injury first appears.
Eelectron microscopy has disclosed the presence of intracytoplasmic lumina within breast cancer cells. These structures can be recognized with the light microscope by their sharp, round outlines and thick walls. Their identification in large numbers may provide additional support for the breast origin of a metastatic tumor. Three illustrative cases in which demonstration of intracytoplasmic lumina was diagnostically helpful are presented.
The findings on rectal biopsy and proctoscopic examination in 23 cases of clindamycin-associated pseudomembranous colitis are summarized. On proctoscopic examination, discrete 2- to 5-mm raised plaques are seen adherent ot an edematous, friable mucosa. Rectal biopsy shows pseudomembrane formation and inflammation of the underlying rectal mucosa. Necrosis of the surface epithelium is a frequent finding; however, true ulcers were not observed. Vasculitis or thrombosis is not a feature of any of the cases. Frequently, the pseudomembrane is observed to be dislodged from the mucosal surface. In five of 23 cases, characteristic pseudomembranes are not present in the biopsy specimen in spite of the fact that they are evident proctoscopically.
Three cases of Hodgkin disease with renal manifestations were studied with electron microscopy and immunofluorescence. The first patient had lipoid nephrosis that disappeared after chemotherapy for Hodgkin disease. Immune-complex nephritis was observed in the second patient who also had Sjogren syndrome. The third patient developed amyloid nephrosis five years after the onset of Hodgkin disease. Apparently, diverse lesions and mechanisms are involved in the development of the nephrotic syndrome in Hodgkin disease and the diagnosis can only be established by appropriate studies of kidney specimens.
The normal luminal surface and the effect of ischemia on the endothelium of the common carotid arteries of rhesus monkeys were examined by scanning electron microscopy. Clamps were placed proximally and distally on the right common carotid arteries, totally occluding the vessels for periods ranging from five minutes to four hours. The clamps were then removed and fixation carried out by intravascular perfusion. The contralateral sham-operated carotids, as well as those from unoperated animals were used as control specimens. The most obvious effect of ischemia was the appearance of conical, crater-like defects in the cytoplasm of endothelial cells. Such "craters" were observed following as little as 15 minutes of ischemia, were much less frequent in sham-operated vessels, and were not seen in the unoperated control specimens.
A peculiar and previously undescribed alteration in the glomerular basement membrane, which we designate as polypoid change, was found in a 4-year-old child with mongolism (trisomy 21). Light and electron microscopical studies were performed. Although the pathogenesis and significance of this lesion remain uncertain, we have compared the lesion with known processes that affect the glomerular basement membrane.
The influence of protein deficiency on the hepatotoxicity of carbon tetrachloride (CCl4) was investigated in a group of rhesus monkeys. Animals fed a protein-rich diet served as controls. The results indicate that protein-deficiency protects the liver against acute hepatotoxicity of this drug. The protective effect is abolished if the animals are administered phenobarbital prior to the administration of CCl4. The protective action is due to a reduction, in protein deficiency, of the endoplasmic reticulum associated enzymes involved in hepatotoxicity of CCl4. Repeated administration of CCl4, which induces hepatic regeneration, resulted in disappearance of fat from periportal cells in protein-deficient animals. The regenerating cells (because of their better enzyme system) acquire "nutritional autonomy" and are thus able to synthesize adequate amounts of lipoproteins for mobilization of liver triglycerides.
Myocardial damage resulting from transthoracic administration of direct current with cardiac defilbrillators present in clinical use was studied in 66 dogs. Electrodes were applied to the thoracic skin. All direct current discharges were delivered via a commercially available defilbrillator. Most of the animals received ten consecutive discharges with a dial setting of 400 watt-seconds. Animals were killed from 3 to 14 days after receiving the discharges. Myocarial necrosis was produced in most of the animals. The lesions were characterized by sharply localized areas of muscle necrosis that progressed to fibrous scars. Mineralization of damaged muscle and florid proliferation of large mononuclear cells were striking features of the lesions.
During investigations of reactive dyes, Levafix Red Violet E-2BL was found suitable for staining of glia fibers. Experiments were carried out on 37% formaldehyde-fixed human autopsy material. Paraffin sections were treated with Luxol Fast Blue MBSN as usual, differentiated until glia fibers were decolorized, and counter-stained in a 0.25% solution of Levafix Red Violet E-2BL in 0.25% acetic acid. Myelin sheaths were colored blue. Gila fibers, smooth muscle cells, and nuclei were stained red violet. Axons and connective tissue remained unstained; occasionally, coarse bundles of collagen showed patchy coloration. Polarization microscopic studies proved that Levafix Red Violet E-2BL is bound to well-oriented fibrous proteins in glia fibers. The similar staining and polarization microscopic properties of glia fibers and smooth muscle support previous findings that glia fibers contain a myosin-like protein.
