Age estimation in children by measurement of open apices in teeth: a study in North Indian population

Age estimation is a prerequisite in forensic medicine, paediatric endocrinology and orthodontic treatment. Dental development has been proven to be suitable for age determination in children because of its lower variability. The aim of this study was to evaluate the applicability of using the open apex method proposed by Cameriere et al. for age estimation in Indian children. Digitalized panoramic radiographs were retrieved from the Department of Oral Medicine & Radiology of 558 Indian children (261 girls, 297 boys) with an age range from 5 to 15 years. The seven left permanent mandibular teeth were evaluated for length and open apices. Dental maturity was evaluated using measurements of the seven left permanent mandibular teeth (x_i = A_i/L_i, i = 1,...,7), the sum of the normalized open apices (s) and the number (N₀) of teeth with root development complete. Using a stepwise multiple regression model, a relationship between open apices, N₀ and age was evaluated. Statistical analysis revealed high accuracy with the morphological variables explaining 88.5% of the variations in estimated chronological age. This research suggests an open apex method could be successful for age estimation in Indian children and could be applied in legal issues pertaining to forensic medicine.     

Was RA Fisher Right?

Randomized controlled trials have become the most respected scientific tool to measure the effectiveness of a medical therapy. The design, conduct and analysis of randomized controlled trials were developed by Sir Ronald A. Fisher, a mathematician in Great Britain. Fisher propounded that the process of randomization would equally distribute all the known and even unknown covariates in the two or more comparison groups, so that any difference observed could be ascribed to treatment effect. Today, we observe that in many situations, this prediction of Fisher does not stand true; hence, adaptive randomization schedules have been designed to adjust for major imbalance in important covariates. Present essay unravels some weaknesses inherent in Fisherian concept of randomized controlled trial.     

Frequency and Factors Associated with Small Intestinal Bacterial Overgrowth in Patients with Cirrhosis of the Liver and Extra Hepatic Portal Venous Obstruction

Spontaneous bacterial peritonitis (SBP), a common complication of cirrhosis of liver, might result from translocation of bacteria from the small bowel. However, there is scanty data on frequency of small intestinal bacterial overgrowth (SIBO) in patients with cirrhosis of the liver. There are no data on SIBO in patients with extra-hepatic portal venous obstruction (EHPVO) in the literature. A total of 174 patients with cirrhosis of the liver, 28 with EHPVO and 51 healthy controls were studied for SIBO using glucose hydrogen breath test (GHBT). Persistent rise in breath hydrogen 12 ppm above basal (at least two readings) was considered diagnostic of SIBO. Of 174 patients (age 47.2 ± 11.9 years, 80.5% male) with cirrhosis due to various causes, 67 (38.5%) were in Child’s class A, 70 (40.2%) class B and 37 (21.7%) class C. Of the 174 patients with cirrhosis, 42 (24.14%) had SIBO as compared to 1 of 51 (1.9%) healthy controls (P < 0.0001). Patients with EHPVO had similar frequency of SIBO compared to healthy controls [2/28 (7.14%) vs 1/51 (1.97%), P = ns]. Frequency of SIBO in Child’s A, B and C was comparable [13 (18.6%) vs 16 (23.9%) and 13 (35.1%), respectively; P = ns]. Presence of SIBO were not related to ascites, etiology of cirrhosis, and degree of liver dysfunction. SIBO is common in patients with cirrhosis of the liver. Patients with EHPVO do not have higher frequency of SIBO than healthy subjects. SIBO in cirrhosis is not related to the degree of derangement in liver function or of portal hypertension.     

Pathological crying as a manifestation of spontaneous haemorrhage in a pontine cavernous haemangioma

A 53-year-old man presented with a sudden onset severe headache associated with ataxia. His family observed labile emotions and frequent episodes of crying. Investigations revealed a pontine cavernoma with evidence of bleeding. The lesion was treated conservatively. Over approximately 6 months, the patient’s ataxia improved and he recovered from the crying episodes. To our knowledge, pathological crying has not been previously associated with brainstem cavernoma.     

JC virus infection in colorectal neoplasia that develops after liver transplantation

PURPOSE: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis. We hypothesized that the use of immunosuppression in LTRs facilitates activation of JCV and is responsible for the increased risk of neoplasia. EXPERIMENTAL DESIGN: JCV TAg DNA and protein expression were determined in normal colonic epithelium (n = 15) and adenomatous polyps (n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40). Apoptosis and proliferation were determined by M30 and Ki-67 immunoreactivity, respectively. RESULTS: JCV TAg DNA was found in 10 of 15 (67%) of normal colonic mucosa from LTRs compared with 5 of 21 (24%) of control normal mucosa (P = 0.025). JCV TAg DNA was detected in 16 of 26 (62%) of the adenomas from LTRs and in 20 of 40 (50%) of control adenomas. JCV TAg protein was expressed in 13 of 26 (50%) adenomas from LTRs versus 2 of 40 (5%) of adenomas from controls (P < 0.001). In adenomas from LTRs, the mean proliferative activity was higher compared with controls (60.3 +/- 3.2% versus 42.7 +/- 2.8%, P < 0.001), whereas mean apoptotic indices were lower in LTRs (0.29 +/- 0.08% versus 0.39 +/- 0.06%, P = 0.05). CONCLUSIONS: The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents, suggests that JCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of colorectal neoplasia in LTRs.