Abstract:

Penetrating ocular trauma frequently causes combined lens and iris tissue injury resulting in traumatic cataract, ectopia lentis, corneal irregularities, traumatic aniridia or irideremia which can be complete or partial, hypoplasia of the iris and loss of iris diaphragm function. The management of patients with co-existing traumatic iris deficiencies and cataract is often challenging due to its heterogeneity, complexity and various associated ocular pathologies. The chief complaints may include photophobia, cosmetic defect, impaired vision and depth of focus. The current various technical options for the treatment of aniridia include iris diaphragm lenses, segmental prosthetic iris devices, flexible iris prosthesis and tinted or painted contact lens /intraocular lens.

We report a case of 44 year old male operated for coexisting traumatic cataract and aniridia by manual sutureless medium incision cataract surgery (MSMICS) and aniridia intraocular lens implantation.

References:

Abstract:

Del cura et al studied the doppler parameters in solid breast lesions and based on that postulated that doppler alone was not a good modality in determining malingancy of a lesion. However the detection of null or reversed diastolic flow on spectral Doppler imaging is an infrequent but highly consistent finding in malignant lesions.

References:

[1.] Chao, T.C., Lo, YF., Chen, S. C., Chen, M. F., (1999). Color Doppler ultrasound in benign and malignant breast tumors: Breast Cancer Res Treat. 57, 193-9.

[2.] Del Cura, J. L., Elizagaray, E., Zabala, R., Legórburu, A., Grande, D., (2005). The Use of Unenhanced Doppler Sonography in the Evaluation of Solid Breast Lesions: Am J Radiol, 184, 1788–1794.

[3.] Dorit, T., Paul, A.L., Jonathan, C,M., Rubin., Quinn-Reidd., (1990). D.Doppler ultrasound colour flow imaging in the study of breast cancers : preliminary findings: Ultrasound Med. Biology, 16, 553-559.

[4.] Lee, W.J., Chu, J.S., Houng, S.J., Chung, M.F., Wang, S. M., Chen, K. M., (1995). Breast cancer angiogenesis: a quantitative morphologic and Doppler imaging study: Ann Surg Oncol, 2, 246-251.

[5.] Moon, W.K., Im, J.G., Noh, D. Y., Han, M. C.,(2000). Nonpalpable breast lesions : evaluation with power doppler US and a microbubble contrast agent – intial experience: Radiology; 217, 240-246.

[6.] Sehgal, C. M., Arger, P.H, Rowling, S. E., Conant, E. F., Reynolds, C., Patton, J. A. (2000). Quantitative Vascularity of Breast Massesby Doppler Imaging: Regional Variations and Diagnostic Implications. J Ultrasound Med, 19, 427-440.

[7.] Stuhrmann, M., Aronius, R., Schietzel, M.,(2000). Tumor Vascularity of Breast Lesions: Potentials and Limits of Contrast-Enhanced Doppler Sonography: Am J Radiol, 175.

[8.] Svensson, W.E., (2002). The use of colour Doppler vascular morphology in improving the ultrasound diagnosis of breast lesions: Acta Clin Croat; (Suppl), 41, 99-100.

[9.] Ueno, E., Tohno, E., Tsunoda-Shimizu, H., Morishima, I. Morphologic Assessment Of Breast Tumors Using Color Doppler Ultrasound. 

Abstract:

The cultivation of human pathogens in experimental animals have made enormous contribution to the understanding and treatment of many diseases of humans. Even though the Mycobacterium leprae was one of the first human bacterial pathogens to be identified, has not been cultivated in vitro till 1960. The long delay in developing appropriate animal models of leprosy, hindered the progress in leprosy research. The long search for an animal model for leprosy has involved almost 30 species of animals and almost as many protocols as research.

References:

[1.] Abstracts from Tropical disease Bulletin, experimental leprosy in monkeys. Indian Journal of Leprosy, V 68(4), 389-390

[2.] Clostan M.J, Adams L.B,(1998) .Report of workshop pathogenesis and lessons from Leprosy. International Journal of Leprosy Dec V 66 (4) P, 597-598.

[3.] Job. C. K., (2000). Developments in experimental Leprosy: Indian Journal of Leprosy, V-72,145-154.

[4.] Peter, A.S., Johnstone, (1987). The search for animal models of leprosy. International Journal of Leprosy, V 55(3), 535-547.

[5.] Rees, R. J. W., (1988). Animal models in Leprosy: British Medical Bulletin V-44/3, 650-664.

[6.] Rees, R. J. W., (1991). Evolution and contribution of animal model in Leprosy: Indian Journal of Leprosy V-63. 446-450.

[7.] Shetty V.P., Anitha N.H (1996). Animal Model For Leprous neuropathy. Indian Journal of leprosy, V 68(1), 95-104.

[8.] Truman R.W, Krahenbul J.L, Viable M.(2001). Leprae as a research reagent. International Journal of Leprosy, March, V 69(1) , 1-12.

Abstract:

 A non randomized ,active controlled trial was done and still is open to recruitment, open label ,phase-1 type among few children over two years of age with positive history of atopy, WALRI and asthma, with intranasal steroid. Intranasal steroid was given in each side of nose with a phial then to follow On Demand Steroid Therapy [ODIST] was advised. Result was noted with their Symptoms Record Book, PEFR, Spirometry and IgE level.

References:

[1.] Andrew, H., Liu Ronina, A.,Covar Joseph, D., Spahn Donald, Y.M., Leung (2007) NHLBI Guidelines for the Diagnosis and Treatment of Asthma Expert Panel Report

[2.] Johns Hopkins. Health Alert: "Asthma and Gastroesophageal Reflux Disease (GERD) -- What's the Connection?". American Academy of Allergy

[3.] Katayoun Bahadori, Mary, M., Doyle-Waters, Carlo Marra, Larry Lynd, Kadria Alasaly, John Swiston and Mark FitzGerald, J (2009). Economic burden of asthma- A systematic review. BMC Pulmonary Medicine, 9(24).

[4.] Kligman,Stanton,Geme S.T.,Schor,Behrman. Chapter 143 – Childhood Asthma. Pediatrics Textbook of Nelson 18th edition

[5.] Louise Chang, M.D. (2012). Asthma & Immunology: "Asthma and GERD,". Gastroesophageal Reflux Disease (GERD)

[6.] Tim Booth, & Nocon Andrew (1991). The Social Impact of Asthma. Family Practice 8 (1), 37-41. 

Abstract:

Diffusion-weighted (DW) MR imaging is a means to characterize and differentiate morphologic features, including edema, necrosis, and tumor tissue, by measuring differences in apparent diffusion coefficient (ADC). These researchers hypothesized that DW imaging has the potential to differentiate recurrent or progressive tumor growth from treatment- induced damage to brain parenchyma in high-grade gliomas after radiation therapy.

References:

[1.] Brandsma, D., Stalpers, L., Taal, W., et al (2008) . Clinical features, mechanisms, and management of pseudoprogression in malignant gliomas. The Lancet Oncology, 9(5), 453-461.

[2.] Brismar, J., Roberson, G.H., Davis, K.R (1976). Radiation necrosis of the brain. Neuroradiological considerations with computed tomography. Neuroradiology, 12(2), 109-113

[3.] Chamberlain, M.C., Glantz, M.J., Chalmers, L., et al (2007) . Early necrosis following concurrent Temodar and radiotherapy in patients with glioblastoma. - Journal of Neuro oncology, 82(1), 81-83.

[4.] Curnes, J., Laster, D., Bal,l M., et al (1986) . MRI of radiation injury to the brain. Am J Roentgenol, 147(1), 119-124.

[5.] Dellen, J.v., Danzinger, A (1978). Failure of computerized tomography to differentiate between radiation necrosis and cerebral tumor. S Afr Med J, 53(5), 171-172.

[6.] Henson, J.W., Ulmer, S., Harris, G.J (2008). Brain tumor imaging in clinical trials. Am J Neuroradiol, 29(3), 419-424.

[7.] Jain, R., Scarpace, L., Ellika, S., et al (2010). Imaging response criteria for recurrent gliomas treated with bevacizumab: Role of diffusion weighted imaging as an imaging biomarker. Journal of Neuro-Oncology ,96(3),423-431.

[8.] Kato, T., Yutaka, S., Tada, M., et al (1996). Long term evaluation of Radiation-induced brain damage by serial magnetic resonance imaging. Neurologia Medico-Chirurgica, 36(12), 870-876.

[9.] Kumar, A.J., Leeds, N.E., Fuller, G.N., et al (2000). Malignant gliomas: MR imaging spectrum of radiation therapy- and chemotherapy-induced necrosis of the brain after treatment. Radiolog, ;217(2), 377-384.

[10.]   Lyubimova, N., Hopewell , J.W, (2004). Experimental evidence to support the hypothesis that damage to vascular endothelium plays the primary role in the development of late radiation-induced CNS injury. Br J Radiol; 77(918), 488-492.

[11.]   Macdonald, D.R., Cascino, T.L., Schold, S.C., et al, (1990). Response criteria for phase II studies of supratentorial malignant glioma. Journal of Clinical Oncology, 8(7), 1277-1280.

[12.]   Mikhael, M. (1978).Radiation necrosis of the brain: correlation between computed tomography, pathology, and dose distribution. J comput Assist Tomogr, 2(1), 71-80.

[13.]   Mullins, M.E., Barest, G.D., Schaefer, P.W., et al (2005). Radiation necrosis versus glioma recurrence: conventional MR imaging clues to diagnosis. AJNR Am J Neuroradiol , 26(8), 1967-1972.

[14.]   Sorensen, A.G., Batchelor, T.T., Wen, P.Y., et al (2008). Response criteria for glioma. Nat Clin Prac Oncol, 5(11), 634-644.

[15.]   Wen P.Y., Macdonald, D.R., Reardon, D.A., et al (2010). Updated response assessment criteria for high-grade gliomas: response assessment in neuro-oncology working group. Journal of Clinical Oncology, 28(11), 1963-1972.

[16.]   Zuniga, R., Torcuator, R., Jain, R., et al (2009). Efficacy, safety and patterns of response and recurrence in patients with recurrent high-grade gliomas treated with bevacizumab plus irinotecan. Journal of Neuro-Oncology, 91(3),329

Abstract:

In 1991, Judah Folkman emphasized the 'angiogenic switch' hypothesis for tumor progression. Studies have showed that angiogenesis positively correlates with the degree of metastasis, tumor recurrence and shorter survival rates, thereby demonstrating the value of angiogenesis as a prognostic cancer marker. Tumor angiogenesis is similar to physiological angiogenesis; however, latter proceeds in an uncontrolled and excessive manner giving rise to leaky and tortuous vessels that are in a constant state of inflammation. As the malignant breast mass grows, tumor cells secrete peptide growth factors, which promote angiogenesis. Angiogenesis, in turn, provides the tumor mass with nutrients essential to sustain growth. In theory, the altered hemodynamics that accompany tumor angiogenesis provide the basis for discriminating between malignant and benign masses of the breast by color Doppler sonography. Lack of smooth muscle in the arteriolar wall and absence of a normal capillary bed results in modified end-organ resistance and arteriovenous shunting.

References:

[1.] Chao, T.C, Lo, Y.F, Chen, S.C, Chen, M.F (1999). Color Doppler ultrasound in benign and malignant breast tumors. Breast Cancer Res Treat, 57 ,193-199.

[2.] Del, Cura, J.L, Elizagaray, E., Zabala, R., Legórburu, A., Grande, D (2005). The Use of Unenhanced Doppler Sonography in the Evaluation of Solid Breast Lesions. Am J Radiol , 184, 1788–1794.

[3.] Dorit, T. P. A.L., Jonathan, C.M., Rubin, Quinn, Reidd, D.(1990). Doppler ultrasound colour flow imaging in the study of breast cancers: preliminary findings. Ultrasound Med. Biol 16, 553-559

[4.] Lee, W.J., Chu, J.S, Houng, S.J., Chung, M.F., Wang, S.M., Chen, K.M.(1995). Breast cancer angiogenesis: a quantitative morphologic and Doppler imaging study. Ann Surg Oncol, 2, 246-251.

[5.] Moon, W.K., I.m J.G., Noh, D.Y., Han, M.C(2000). Nonpalpable Breast Lesions: Evaluation with Power Doppler US and a Microbubble Contrast Agent—Initial Experience. Radiology, 217,240–246.

[6.] Sehgal, C.M, Arger, P.H, Rowling, S.E, Conant, E.F, Reynolds, C., Patton, J.A (2000). Quantitative Vascularity of Breast Massesby Doppler Imaging: Regional Variations and Diagnostic Implications. J Ultrasound Med, 19:427–440.

[7.] Stuhrmann, M., Aronius, R., Schietzel, M. (2000). Tumor Vascularity of Breast Lesions: Potentials and Limits of Contrast-Enhanced Doppler Sonography . Am J Radiol 175.

[8.] Svensson, W.E (2002). The use of colour Doppler vascular morphology in improving the ultrasound diagnosis of breast lesions ; Acta Clin Croat, 41 (Suppl), 99-100.

[9.] Uen,o E., Tohno, E., Tsunoda-Shimizu, H. , Morishima, I. Morphologic assessment of breast tumors using color doppler ultrasound 

Abstract:

Fat embolism syndrome (FES) occurs when embolic fat macro globules pass into the small vessels of the lung and other sites, producing endothelial damage and resulting respiratory failure (ARDS-like picture), cerebral dysfunction and a petechial rash. The incidence of fat emboslism in all kinds of fractures is about 16% but sometimes it is as high as 50% to 62%. The fat embolism is common in fatty and bed ridden patients and in whom reamed interlocking is performed under tourniquet and surgery is to be delayed. But in the case discussed by us unreamed interlocking was performed without tourniquet and the operative procedure was done within 4 hours after trauma and the pre-operative investigation were within normal limits. Patient was lean and thin. The present case report is discussed to convey the message that even when surgeon takes every precaution for prevention of fat embolism, it can occur in any case.

References:

[1.] Tzun, Tsai, Chin-Jung, Hsu, Ying-Hao, Chen, Yi-Chin, Fong, Horng-Chaung, HSU, et al (2010). Fat Embolism syndrome in long bone fracture – clinical experience in a terliary referral center in Tawian. Journal of the Chines Medical Association, 73 (8), 407-410.

[2.] James ,C., Glazer, & Danie,l K., Orian. Fat embolism syndrome in a surgical Patient. JABFP, vol 14, No. 4.

[3.] Stein, P.D., Yaekoub, A.Y, Matta, F., et al (2008). Embolism syndrome. Am J Med Sci, 336(6), 472-477.

[4.] Taviloglu, K., Yanar, H. (2007). Fat embolism syndrome. Surg Today, 37(1), 5-8.

[5.] Tumerdem, B., Onel, D., Topalan, M., Korpinar, S., Aktas, S (2008) Fat embolism syndrome after lower extremity replantation associated with libia fracture : case report. Ulus Travma. Acil Cerrahi Derg, 14(1), 73-75.