Graphene nanoplatelets as nanofillers in mesoporous silicon oxycarbide polymer derived ceramics.

Understanding the role of graphene in the thermal stability and pore morphology of polymer derived silicon oxycarbide is crucial for electrochemical energy storage and hydrogen storage applications. Here in this work, we report the synthesis of graphene nanoplatelets dispersed silicon oxycarbide ceramics by the polymer to ceramic synthesis route. Samples containing graphene and without graphene are subjected to different pyrolysis conditions and are characterized using FT-IR, XPS, Raman spectroscopy, XRD, FE-SEM, HR-TEM, and BET. The results show that the graphene dispersed in the ceramic has undergone structural distortions upon pyrolysis and resulted in the formation of nanoclusters of graphene and turbostratic graphene. The XRD results confirm that with the incorporation of higher wt.% of GNP there is resistance to crystallization even at an exceedingly high pyrolysis temperature. The pores are bimodal in nature with specific surface area ranging between 22 and 70 m2/g and are generated in-situ during the polymer to ceramic conversion. Our study confirms that upon adjusting the graphene content it is possible to tune the structure and pore morphology of the polymer derived ceramics as per the requirements.

Desmoid tumour: a rare etiology of intestinal obstruction.

Intestinal obstruction is a frequently encountered entity in surgical practice. The signs & symptoms, many a times, are suggestive of the level of obstruction, making the diagnosis of obstruction evident. There are various causes of intestinal obstruction which diversify to an enormous extent, stamping on the famous paradigm for the mysterious nature of the abdomen being referred to as the Pandora's Box. In accordance with the above saying, we report a rare case of a desmoid tumour, presenting as intestinal obstruction, which entices us to strongly believe the same.

Eugenia jambolana pretreatment prevents isoproterenol-induced myocardial damage in rats: evidence from biochemical, molecular, and histopathological studies.

Preventive effects of hydroalcoholic extract of fruit pulp of Eugenia jambolana (HEEJ) on isoproterenol (ISP)-induced myocardial damage in rats were evaluated. Rats were pre-treated with HEEJ (100, 200, and 400 mg/kg) daily for 30 days. ISP (85 mg/kg bw) was administered on the 28th and 29th days at an interval of 24 h. Ischemic control group exhibited significant increases in oxidative stress parameters, markers of inflammation, cardiac damage markers, and apoptotic markers. Oral pre-treatment with HEEJ (100, 200, and 400 mg/kg bw) provided cardioprotective activity by decreasing levels of malondialdehyde, cardiac markers (serum glutamate oxaloacetate transaminase, creatine kinase-myocardial band, cardiac troponin I), and markers of inflammation (interleukin-6, C-reactive protein, and tumor necrosis factor alpha); and increased levels of superoxide dismutase and reduced glutathione. HEEJ (400 mg/kg bw) was found to exert significantly greater effects in comparison to HEEJ (100 and 200 mg/kg bw). Apoptotic marker Bcl-2 was increased, while Bax was decreased in pre-treated rats, which was further confirmed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. The present study provides evidence that pre-treatment with HEEJ attenuates oxidative stress, apoptosis and improves cardiac architecture in ISP-induced rats and, hence, is cardioprotective.

N-acetyl-L-cysteine modulates multiple signaling pathways to rescue male germ cells from apoptosis induced by chronic hCG administration to rats.

The present study was aimed to investigate the beneficial effects of N-acetyl-L: -cysteine (NAC, 150 mg/kg bw twice/week) against testicular germ cell apoptosis in rats induced by chronic hCG administration (100 IU/rat/day for 30 days). NAC co-treatment improved serum testosterone, prevented rise in lipid peroxidation, intracellular H(2)O(2) and the activities of antioxidant enzymes in germ cells. Replenishment of intracellular GSH and total antioxidant capacity was seen. There was a marked reduction in TUNEL positive germ cells and expression of caspase-3 (p < 0.01) and PARP cleavage. Pro-apoptotic markers Fas, FasL, caspase-8 were also significantly downregulated. While Bcl-2 was fully restored, rise in Bax, caspase-9, phospho-JNK/JNK and phospho-c-Jun/c-Jun expression was significantly arrested. Anti-apoptotic phospho-Akt/Akt and NF-κB were otherwise found upregulated. Taken together, the above findings demonstrate that NAC intervention rescued the testicular germ cells from demise following chronic hCG treatment through regulation of multiple signaling mechanisms of metazoan apoptosis.

Differential modulation of apoptotic gene expression by N-acetyl-L-cysteine in Leydig cells stimulated persistently with hCG in vivo.

The present study was designed to investigate the molecular mechanisms of NAC (150 mg/kg bw twice/week) action in vivo under repeated hCG (100 IU/rat/day) stimulation to adult rats. Leydig cell refractoriness led to a significant decline in serum testosterone and intracellular cAMP by day 30 of chronic hCG intervention which improved significantly following NAC co-administration. It inhibited the rise in lipid peroxidation, improved the activity of antioxidant enzymes along with intracellular glutathione and total antioxidant capacity in the target cells. Leydig cell apoptosis declined significantly (P<0.001) with down-regulation of upstream, Fas, FasL, caspase-8, Bax and caspase-9, JNK/pJNK and downstream caspase-3 and PARP. On the other hand, anti-apoptotic Bcl2, NF-kß, and Akt were up-regulated. Taken together, the above findings indicate that the specificity of NAC action was not restricted to regulating marker proteins in the extrinsic and JNK pathways as seen in vitro but extended to include intrinsic pathway of metazoan apoptosis as well.

A prospective single center study to assess the impact of surgical stabilization in patients with rib fracture.

OBJECTIVE: To compare the intensity of pain and duration of return to normal activity in patients with rib fractures treated with surgical stabilization with plating versus conventional treatment modalities. PATIENTS AND METHODS: This study was conducted over a 12 month period. Patients with rib fractures were assessed by numerical pain scale. Patients having pain scale less than 5 were excluded from study. Patients having pain scale of 5 or more than 5 were treated with conventional treatment for next 10 days. On 11th day patients were again assessed by numerical pain scale and patients having score less than 5 were excluded from study. Patients having pain scale of 5, 6, and 7 were treated with conventional treatment and patients having pain scale of 8, 9, and 10 were selected for operative management. Operative and control group were compared on basis of intensity of pain and duration of return to normal activity. Follow up was done on 5, 15, and 30 post operative day. RESULTS: There was less pain in operative group as compared to control group. Mean rib fracture pain in operative group was 9.15, 2.31, 1.12 as compared to 6.25, 5.96, 4.50 in control group on 5, 15 and 30 post operative days. Also there was early return to normal activity in operative group. CONCLUSION: Surgical stabilization of rib fracture, an underutilized intervention is better than conventional conservative management in terms of both, decrease in intensity of pain and early return to normal activity.

N-acetyl-L-cysteine counteracts oxidative stress and prevents H2O2 induced germ cell apoptosis through down-regulation of caspase-9 and JNK/c-Jun.

The mechanism of H(2)O(2) induced oxidative stress leading to male germ cell apoptosis was earlier reported from our laboratory. In the present study, we investigated the mechanisms by which N-acetyl-L-cysteine (NAC, which is highly cell specific with strong antioxidant and anti-genotoxic properties), stimulated cell survival under such conditions. Co-incubation with 5 mM NAC significantly (P<0.001) reduced the germ cell apoptosis induced by 10 µM H(2)O(2). Lipid peroxidation was brought down with significant restoration of activities of antioxidant enzymes, SOD, GST, and catalase. Expression of pro-apoptotic marker, Bax up-regulated following H(2)O(2) exposure, was reversed back to control levels. In contrast, expression of anti-apoptotic Bcl-2 and phospho-Akt revealed a completely opposite trend. While caspase-8 activity remained unaffected, NAC successfully attenuated the increased activities of caspase-3 and -9 in the H(2) O(2) treated cells. Simultaneously, the increased expression of caspase-9, phospho-JNK, and phospho-c-Jun after H(2)O(2) treatment was down-regulated by NAC. The above findings indicate that the mechanism of inhibition of H(2)O(2) induced male germ cell apoptosis by NAC is mediated through regulation of caspase-9 and JNK.

N-acetylcysteine counteracts oxidative stress and prevents hCG-induced apoptosis in rat Leydig cells through down regulation of caspase-8 and JNK.

We have earlier reported that following persistent stimulation with hCG, oxidative stress-induced apoptosis in rat Leydig cells was mainly achieved through the extrinsic pathway. In the present study, the role of N-acetylcysteine (NAC) in counteracting the oxidative stress and the mechanisms of inhibition of apoptosis under such conditions were investigated. NAC (1 mM) intervention with repeated hCG stimulation (50 ng/ml, four times, each with 30 min challenge) prevented the decline in Leydig cell viability and the rise in lipid peroxidation and reactive oxygen species. Simultaneously, the activities of the enzymes glutathione-S-transferase, catalase, superoxide dismutase and the intracellular glutathione and antioxidant capacity of the treated cells improved significantly. Apoptotic markers Fas, FasL, and caspase-8, up-regulated following repeated hCG exposure, were significantly down-regulated following NAC co-incubation. While Bcl-2 expression was fully restored, Bax and caspase-9 remained unchanged. NAC treatment induced down-regulation of upstream JNK/pJNK and down-stream caspase-3 in the target cells. Taken together, the above findings indicate that NAC counteracted the oxidative stress in Leydig cells induced as a result of repeated hCG stimulation, and inhibited apoptosis by mainly regulating the extrinsic and JNK pathways of metazoan apoptosis.

Rare asymptomatic presentations of schwannomas in early adolescence: three cases with review of literature.

INTRODUCTION: Schwannoma also known as Neurilemoma is a benign neoplasm of the Schwann Cells of the neural sheath. They are usually found to occur in the extremities, but can also be found in the trunk, head and neck, pelvis, and rectum. It is seldom painful and usually remains small. It has no potential for malignancy unless the patient has multi-neural tumours. It usually presents as a slowly enlarging painless nodule somewhat movable beneath the surface, rarely becomes larger than 2cm in diameter and is most frequently diagnosed in 25-55 yrs of age. PATIENTS AND METHODS: We report three rare, asymptomatic presentations of schwannomas at adolescent age, in the back, pancreas and in the cervical region with a review of the available literature. CONCLUSION: Despite the rarity of the presentations, as encountered by us, similar swellings in the adolescent age group can be schwannomas and can be adequately managed surgically alone. This is what should be borne in mind, for 'what the mind knows is what the eyes see'.

Adverse effects associated with persistent stimulation of Leydig cells with hCG in vitro.

The detrimental effects of persistent stimulation with hCG were investigated in rat Leydig cells in vitro. Significant rise in lipid peroxidation and reactive oxygen species (ROS) with concomitant attenuation in the activities of antioxidant enzymes: superoxide dismutase, catalase, and glutathione-S-transferase was observed. Transcripts for catalase and superoxide dismutase were also depleted. Subsequent to each hCG challenge, the total antioxidant capacity in the target cells also declined significantly (P < 0.05). There was an increase in cell apoptosis (23%), which was associated with a rise in caspase-3 activity, PARP cleavage, and Fas, FasL, caspase-8 expression. While Bax and Caspase-9 expression remained unchanged, Bcl-2 demonstrated a marked decline. Taken together, the above data indicate that persistent hCG stimulation of Leydig cells induced adverse effects leading to oxidative stress and apoptosis which was channeled primarily through the extrinsic pathway.

Pathways involved in testicular germ cell apoptosis induced by H2O2 in vitro.

H(2)O(2) induces apoptosis in variety of cells; however, the sensitivities of testicular germ cells to H(2)O(2) are not known. In the present study, H(2)O(2), at concentrations in the range 1-10 microM, was found to induce apoptosis in testicular germ cells in vitro. Following 1 h of treatment with 10 microM H(2)O(2), a 10-fold rise in the percentage of apoptotic cells was observed. Induction of germ cell apoptosis was directly associated with a significant (P < 0.01) increase in lipid peroxidation and a concomitant decrease in superoxide dismutase and catalase activity. Examination of apoptotic signalling pathways revealed an increased expression of extrinsic (Fas, FasL and caspase-8) and intrinsic (Bid, Bak, Bad, Bax and caspase-9) markers, as well as p53, along with a simultaneous decrease in the Bcl-2 protein at the highest concentration of H(2)O(2) exposure. Both, c-jun N-terminal kinase and p38 phosphorylated forms were found to be up-regulated. Interestingly, up-regulation of the nuclear transcription factor kappa B was also observed. The respective transcripts for many of the above proteins followed an identical trend. Caspase-3 activity was also estimated to be 30-fold higher. Taken together, the above data indicate that testicular germ cells are prone to apoptosis at very low concentrations of H(2)O(2), the mechanism of which involves extrinsic and intrinsic as well other regulatory pathways.