On the sensitivity of thermophotonic lock-in imaging and polarized Raman spectroscopy to early dental caries diagnosis.

Dental caries is the leading cause of tooth loss, which can promptly be prevented if detected in early stages of progression. Unfortunately, conventional diagnostic modalities currently used in dentistry lack the sensitivity to detect early caries. The authors' intention is to compare the ability of polarized Raman spectroscopy and thermophotonic imaging to make early caries diagnosis. Extracted human teeth with no visible stain or defects were artificially demineralized in accordance to a well-known protocol in dentistry for simulated early caries development at several demineralization stages. Samples were then inspected using polarized Raman spectroscopy and thermophotonic imaging. The sensitivities of these two diagnostic modalities are compared, and the results are verified using transverse micro-radiography. It was found that compared to polarized Raman spectroscopy, thermophotonic imaging exhibits superior sensitivity to very early stages of demineralization.

The study of tooth wear patterns and their associated aetiologies in adults in Kelantan, Malaysia

Tooth wear is the loss of tooth tissue and structures not due to caries. It can occur in various forms either attrition, abrasion, erosion, noncaries cervical lesion (NCCL) or a combination of two or more forms. The objective of this study was to determine the patterns and associated aetiologies of tooth wear among adults in Kelantan, Malaysia. This crosssectional study involved 81 adults with tooth wear which was visually assessed using the Smith and Knight Tooth Wear Index (TWI). A questionnaire was used to seek putative aetiologies of the wear. Data were analyzed and the results were expressed as frequencies and percentages. Six thousand three hundred and eighty four tooth surfaces were examined in 1596 teeth. 17.4% surfaces had tooth wear; 80% scored 1, 18% scored 2 and 2% scored 3. Among the 81 cases of tooth wear, 29 (35.8%) had abrasion; 25 (30.9%) had attrition; 1(1.2%) had erosion while 26 (32.1%) had the combined type. Among those with abrasion, majority had the habit of eating freshwater clams (Corbicula fluminea) as local delicacy where most of the times people use their teeth to pry open the clam shells. Erosion was related to the pooling of carbonated drinks or beverages in the mouth before swallowing. In conclusion, most adults experienced abrasion and the most common possible associated aetiology is the way of eating clams.

Selective neuroprotective effects with insulin-like growth factor-1 in phenotypic striatal neurons following ischemic brain injury in fetal sheep.

Severe perinatal asphyxia can lead to injury and dysfunction of the basal ganglia. Post insult administration of insulin-like growth factor-1 is neuroprotective, particularly in the striatum. Insulin-like growth factor-1 is also known to be a neuromodulator of several types of striatal neurons. The striatum comprises various phenotypic neurons with a complex neurochemical anatomy and physiology. In the present study, we examined the specificity of neuronal rescue with insulin-like growth factor-1 on different striatal neurons. Bilateral brain injury was induced in near term fetal sheep by 30 min of reversible carotid artery occlusion. A single dose of 3 microg of insulin-like growth factor-1 was infused over 1 h into the lateral ventricle 90 min following ischemia. The histological and immunohistochemical outcome were examined after 4 days recovery using paraffin tissue preparations. Insulin-like growth factor-1 treatment (n = 11) significantly reduced the percentage of neuronal loss in the striatum compared with the vehicle treated group (n = 10, 28.3+/-5.1% vs 55.5+/-17.3%, P < 0.005). Immunohistochemical studies showed that ischemia resulted in a significant loss of calbindin-28kd, choline acetyltransferase, parvalbumin, glutamate acid decarboxylase, neuronal nitric oxide synthase and neuropeptide Y immunopositive neurons, compared with sham controls. Insulin-like growth factor-1 markedly prevented the loss of calbindin-28kd (n = 7, P < 0.05), choline acetyltransferase (n = 7, P < 0.05), neuropeptide Y (n = 7, P < 0.05), neuronal nitric oxide synthase (n = 8, P < 0.05) and glutamate acid decarboxylase (n = 9, P < 0.05) immunopositive neurons, but failed to protect parvalbumin (n = 6) immunopositive neurons. The present study indicates that the therapeutic effect of insulin-like growth factor-1 in the basal ganglia is selectively associated with cholinergic and some phenotypic GABAergic neurons. These data suggest a potential role for insulin-like growth factor-1 in preventing cerebral palsy due to perinatal asphyxia.

LPS pretreatment reprograms macrophage LPS-stimulated TNF and IL-1 release without protein tyrosine kinase activation.

Pretreatment of macrophages with low-dose endotoxin (LPSp) profoundly alters cytokine release in response to subsequent LPSa activation. These qualitative and quantitative alterations in cytokine release have been termed macrophage reprogramming. Macrophage activation by LPS is thought to occur via a mechanism involving an early protein tyrosine kinase (PTK) phosphorylation step. PTK inhibition with genistein or herbimycin A blocks LPSa-stimulated secretion of tumor necrosis factor (TNF) and interleukin-1 (IL-1). In this study we investigated whether a PTK pathway participates in LPSp pretreatment reprogramming. We show that LPSp pretreatment inhibited TNF and augmented IL-1 release in response to subsequent LPSa stimulation. Blockade of PTK activation pathways during the interval when macrophages were exposed to LPSp prevented mitogen-activated protein kinase phosphorylation, as well as LPSp-stimulated release of TNF and IL-1, but did not block LPSp reprogramming effects. We conclude that LPSp pretreatment reprogramming of macrophage cytokine production does not require PTK activation.

Reprogrammed macrophage tumor necrosis factor and interleukin-1 release with inflammatory pretreatment: differential regulation by endotoxin and zymosan.

OBJECTIVE: To determine whether different reprogrammed alterations in endotoxin (lipopolysaccharide, LPS)-stimulated tumor necrosis factor (TNF) and interleukin-1 (IL-1) release are seen following pretreatment with endotoxin (LPSp) or pretreatment with the particulate inflammatory stimulus zymosan. METHODS: Murine peritoneal macrophages (M phi) pretreated for 24 hours in vitro with medium, LPSp, zymosan, latex beads, or killed Escherichia coli. After 24 hours M phi were restimulated with medium, LPSa, zymosan, latex beads, or E. coli, M phi supernatant TNF and IL-1 were measured after 24 hours and mRNA levels determined after 6 hours with reverse-transcriptase polymerase chain reaction. RESULTS: Pretreatment with low dose LPSp markedly inhibited TNF release by both LPSa or zymosan, while pretreatment with zymosan increased LPSa-stimulated TNF release. Pretreatment with both LPSp and zymosan augmented LPSa and zymosan-stimulated IL-1. Zymosan pretreatment augmentation of TNF and IL-1 was accompanied by lower than basal levels of cytokine message. CONCLUSION: Reprogrammed macrophage TNF and IL-1 release was differentially regulated by distinct inflammatory stimuli. Understanding reprogrammed macrophage cytokine regulation may enable specific therapy to modify dysregulated cytokine release during sepsis and trauma.

Macrophage endotoxin tolerance. Tumor necrosis factor and interleukin-1 regulation by lipopolysaccharide pretreatment.

OBJECTIVE: To correlate cytokine gene expression with the release of protein product by murine peritoneal macrophages rendered tolerant by sequential endotoxin stimulation in vitro. DESIGN: In vitro investigation of the regulation of endotoxin-stimulated cytokine production following endotoxin pretreatment using cytokine bioassays, polymerase chain reaction, and Northern blot analyses. SETTING: In vitro cell culture model of sequential endotoxin stimulation of murine macrophages. INTERVENTIONS: Macrophages were pretreated with 0 or 100 ng/mL of lipopolysaccharide (LPS1) for 24 hours and then stimulated with 0 or 100 ng/mL of LPS (LPS2) for 4 or 24 hours. After stimulation, supernatant tumor necrosis factor (TNF) and interleukin-1 (IL-1) levels were measured by bioassay. Total RNA was extracted and messenger RNA (mRNA) corresponding to TNF and IL-1 was amplified by reverse transcription-polymerase chain reaction or analyzed by Northern blot. RESULTS: Endotoxin pretreatment resulted in the augmentation of IL-1 (mean +/- SD, 78 +/- 9 vs 596 +/- 42 pg/mL, P < .01) and the inhibition of TNF (274 +/- 63 vs 61 +/- 3 pg/mL, P < .01) release 4 hours after stimulation with 100 ng/mL of LPS2. A similar pattern of cytokine release was observed 24 hours after LPS2 stimulation. Pretreatment produced an increased IL-1 message in response to 100 ng/mL of LPS2. The TNF message was detectable in all groups receiving LPS2 alone, but the highest levels of TNF mRNA were seen in LPS1-pretreated cells stimulated with LPS2. CONCLUSIONS: Endotoxin pretreatment produced increased IL-1 message that paralleled the augmentation of IL-1 protein, whereas abundant TNF message was present even though TNF protein release was significantly inhibited. In this model of in vitro endotoxin tolerance, pretreatment initiates divergent pathways of cytokine regulation.

Diabetic impotence: studies of nocturnal erection during REM sleep.

Nocturnal erections were studied in 30 diabetic patients who complained of impotence and in 11 healthy volunteers. The maximum increase in penile circumference was measured by a penile strain-gauge and recorded on a portable tape-recorder; an external oculogram was recorded simultaneously to identify periods of rapid-eye-movement sleep. The technique gave reproducible results, was acceptable to patients, and was suitable for use in an oridnary hospital ward. Only six diabetics showed a maximum increase in penile circumference of under 15 mm, whereas all but one of the healthy subjects showed maximum increases above this value. Of the six diabetics, five complained of total impotence and had other features of autonomic neuropathy that suggested an organic basis for their impotence. The other patient complained of partial importence, which was probably caused by psychological factors. These findings suggest that the prevalence of organic impotence among diabetics has been overestimated.