GALLBLADDER POLYPS: FACTORS AFFECTING SURGICAL DECISION.

Abstract

AIM: To determine the factors affecting the decision to perform surgery, and the efficiency of ultrasonography (USG) in detecting gallbladder polyps (GP).

METHODS: Data for 138 patients who underwent cholecystectomy between 1996 and 2012 in our clinic with a diagnosis of GP were retrospectively analyzed. Demographic data, clinical presentation, principal symptoms, ultrasonographic and histopathological findings were evaluated. Patients were evaluated in individual groups according to the age of the patients (older or younger than 50 years old) and polyp size (bigger or smaller than 10 mm) and characteristics of the polyps (pseudopolyp or real polyps). χ2  tests were used for the statistical evaluation of the data.

RESULTS: The median age was 50 (26-85) years and 91 of patients were female. Of 138 patients who underwent cholecystectomy with GP diagnosis, only 99 had a histopathologically defined polyp; 77 of them had pseudopolyps and 22 had true polyps. Twenty-one patients had adenocarcinoma. Of these 21 patients, 11 were male, their median age was 61 (40-85) years and all malignant polyps had diameters > 10 mm (P< 0.0001). Of 138 patients in whom surgery were performed, 112 had ultrasonographic polyps with diameters < 10 mm. Of the other 26 patients who also had polyps with diameters > 10 mm, 22 had true polyps. The sensitivity of USG was 84.6% for polyps with diameters > 10 mm (P < 0.0001); however it was only 66% in polyps with diameters < 10 mm.

CONCLUSION: The risk of malignancy was high in the patients over 50 years old who had single polyps with diameters >10 mm.

 

Core tip: Early stage gallbladder cancers can often be detected as polyps in imaging studies. The aim of this study was to determine the factors affecting surgery by analyzing the incidence of malignancy of gallbladder polyps (GP) and the efficiency of ultrasonography in detecting GP. Of 138 patients with GP on imaging, 99 had polyps and 21 had histopathologically confirmed adenocarcınoma. Of these 21 patients, all malignant polyps were solitary and had a diameter >10 mm. In our study, the risk of malignancy correlated wıth age over 50 years old, solitary polyp and polyp diameter >10 mm.

 

Key words: Gallbladder; Polyps; Ultrasound; Cholecystectomy; Malignancy

 

© 2013 Baishideng. All rights reserved.

 

GASTRIC DUPLICATION CYST @ MEDIC

Male patient 26yo from An Giang province complaints of nausea. Endoscopy revealed a submucosa mass at posterior antrum, which was confirmed later by CT,  but cannot rule out a heterotopic pancreas.

Ultrasound detected a cystic mass from greater curvature which has cyst wall like gastric wall and no debris inside.

Transversal section at antrum= Water filling helps viewing clearly root of gastric duplication cyst which continued greater curvature of stomach. The cyst wall has 2 layers: hypoechoic muscularis and hyperechoic lining mucosa [muscular rim].  

Our present case has these criteria : (a) the wall of the cyst is contiguous with the stomach wall; (b) the cyst is surrounded by smooth muscle, which is continuous with the muscle of the stomach; and (c) the cyst wall is lined by epithelium of gastric or any other type of gut mucosa.

The gastric duplication cyst has clearly muscular rim with size of 27.1x15.6mm without debris inside.

The hypoechoic muscularis of the gastric antrum appears to be contiguous with the hypoechoic rim of the cystic lesion (white arrow).

A video clip of gastric duplication cyst on ultrasound examination.

So it is a noncommunicating gastric duplication cyst with the gastric lumen. Patient underwent surgery to remove the gastric duplication cyst on 20/8/2013 with the normal pathological report. After 3 months of operation he remains well and endoscopy shows a gastric scar on posterior surface of his stomach.

_________________________________

Explanation (from Chavira, http://pediatricimaging.wikispaces.com/Chavira-001-Gastric+Duplication+Cyst)

Gastrointestinal duplication cysts occur in 1 in 4500 births, of these 75% are intraabdominal, 20% thoracic, and 5% thoracoabdominal. Gastric duplication cysts, in particular, are one of the most rare comprising 7% of all gastrointestinal cysts. Other locations include the jejunum/ileum (53%), esophagus (18%), colon (13%), and duodenum (6%). Gastric duplication cysts are often a missed diagnosis because of their rarity and vague clinical presentation.

Duplication cysts arise due to a congenital developmental abnormality within the gastrointestinal tract, of which the etiology is not completely understood. Multiple theories have been developed to explain their existence including partial twinning, in utero ischemic events, and abnormal endoderm and notochord separation. Bremer's theory of abnormal recanalization has also been described to explain their occurrence. A brief review of the embryology related to the development of the alimentary tract helps to better understand this theory.

During the 6th week of gestation, epithelial cells proliferate and the lumen of the GI tract becomes occluded. Vacuoles are then created which fuse with one another to recanalize the lumen. Abnormal development of the gastrointestinal lumen can occur when a group of vacuoles coalesce with one another but do not form a connection with the developing lumen, with continued growth a wall of bowel will then form between them, which may lead to the formation of a duplication cyst not in communication with the gastric lumen. Conversely, if a small group of vacuoles coalesce and one opens into the main lumen, the duplication cyst may form in communication with the gastric lumen. 

Image 1. Normal and abnormal development of the gastrointestinal lumen are depicted in the above image.

It is important to note that although each theory offers an explanation for the formation of duplication cysts, there is no singly theory that can adequately explain the occurrence of all forms of duplication cysts.

The presentation of duplication cyst depends on the size and location. The typical presentation is in a child less than 2 years of age with females being more commonly affected than males. However, adult cases have been reported. The typical symptoms are nausea, vomiting, and a palpable abdominal mass. However, in some cases patients may be entirely asymptomatic. The features characteristic of a duplication cyst include a well-developed coat of smooth muscle, an epithelial lining the same as that of the alimentary tract, and an attachment or prior attachment to a part of the alimentary tract. The location of the cyst is typically along the greater curvature and most are not in communication with the gastric lumen.

The diagnosis of a duplication cyst is usually made with CT and US imaging. Ultrasound is becoming the preferred diagnostic imaging tool, as in some cases it may reveal the "double wall sign" outlining the echogenic inner layer and hypoechoic outer muscular layer which is characteristic of a duplication cyst. In some cases, however, imaging is not sufficient and the diagnosis is confirmed intraoperatively.

Treatment for gastric duplication cyst is surgical. The excision of a gastric duplication cyst can usually be done with minimal loss of adjacent stomach. However, if the duplication cyst and gastric lumen are in communication, partial gastrectomy is required. Complications that may occur if untreated include perforation and ulceration. There is also a risk of malignant transformation.

_________________________________

 From Review of Radiology, DAHNERT.

Gastric duplication cyst = intramural gastric cyst lined with secretory epithelium

Incidence: 7% of all alimentary tract duplications

Path: noncommunicating spherical cyst (majority); may communicate with aberrrant pancreatic duct; ectopic pancreatic tissue found in 37%

Symptomatic age: infancy; in 75% detected before age 12; M:F = 1:2

• pain (from overdistension of cyst, rupture with peritonitis, peptic ulcer formation, internal pancreatitis)

• vomiting, anemia, fever

• symptoms mimicking congenital hypertrophic pyloric stenosis (if duplication in antrum / pylorus)

Most common site: greater curvature (65%)

- paragastric cystic mass up to 12 cm in size, indenting greater curvature

- seldom communicates with main gastric lumen at one or both ends

- may enlarge + ulcerate

- Tc-99m uptake



US:

+ cyst with two wall layers (inner echogenic layer of mucosa, outer hypoechoic layer of muscle)

+ clear / debris-containing fluid


Cx:

(1) Partial / complete small bowel obstruction

(2) Relapsing pancreatitis (with ductal communication)

(3) Ulceration, perforation, fistula formation

DDx: pancreatic cyst, pancreatic pseudocyst, mesenteric cyst, leiomyoma, adenomatous polyp, hamartoma, lipoma, neurofibroma, teratoma

Discussion

Gastrointestinal duplication is a relatively rare anomaly that may occur at any level from oral cavity to rectum with ileum being the most common site. Duplication cysts of the stomach are quite rare, and most of them have been reported in children [1, 5, 6]. Duplication cysts of ileum are usually located on mesenteric border [7], whereas the usual location for gastric duplication cysts is along the greater curvature [4, 6, 7]. The duplication cyst is entirely separated from the adjacent bowel but shares a common wall [8].The essential criteria for diagnosis of a gastric duplication cyst are (a) the wall of the cyst is contiguous with the stomach wall; (b) the cyst is surrounded by smooth muscle, which is continuous with the muscle of the stomach; and (c) the cyst wall is lined by epithelium of gastric or any other type of gut mucosa [1, 4, 9].

Our present cases fulfilled these criteria excluding other diagnoses.

Gastric duplication cysts comprise 4% of all gastrointestinal duplications. Various other congenital anomalies such as alimentary tract duplications, esophageal diverticulum, or spinal cord abnormalities are encountered in up to 50% patients [8]. These malformations are believed to be congenital, formed before the differentiation of epithelial lining, and therefore named for the organ with which they are associated [3, 10]. Duplications result from the disturbances in embryonic development, and various theories have been proposed for the actual mechanism. Bremer proposed the theory of errors of recanalization and fusion of longitudinal folds. He suggested that duplication cysts originated from the fusion of longitudinal folds allowing the passage of a bridge of submucosa and muscle at the second and third month of intrauterine life [5]. McLetchie suggested that adhesion of notochord and embryonic endoderm might not elongate as quickly as its surrounding structures, causing traction diverticulum leading to duplication cyst formation [5]. Other theories of enteric duplication include abortive twinning, persistent embryological diverticula, and hypoxic or traumatic events [5]. There is no single theory that is satisfactory for all types of duplications [5].

Greater than 80% of gastric duplications are cystic and do not communicate with lumen of the stomach. The remainders are tubular with some communication [5]. The structure is defined as tubular when the lumen is contiguous and cystic when the lumen is not contiguous with stomach lumen [6]. The mucosal lining of duplication may be histologically similar to the segment of gut to which is topographically related.

However, some duplications may include lining from other segment of alimentary or respiratory tract. The presence of respiratory epithelium in the cysts of thorax, tongue, liver, and stomach suggests that the undifferentiated epithelium of foregut might undergo transition to differentiated specialized epithelium during embryonic period [5].

Gastric duplications typically become symptomatic during childhood. 67% are diagnosed within the first year of life, and less than 25% are discovered after age 12 [4]. The duplication cysts of the stomach are usually diagnosed intraoperatively in adults [10]. In our first patient, the preoperative CT and MRI findings were interpreted as being most consistent with a pancreatic neoplasm, and diagnosis of GDC was suspected only during surgery. The clinical presentation of gastric duplication cysts can be highly variable and nonspecific ranging from vague abdominal pain to nausea, vomiting, epigastric fullness, weight loss, anemia, dysphagia, dyspepsia with abdominal tenderness and epigastric mass on physical examination [4,10]. Because most cases occur along the greater curvature of the stomach, the cysts can potentially compress the adjacent organs such as pancreas, kidney, spleen, and adrenal gland. Accordingly, the differential diagnosis would include lesions arising from these organs [2]. The cysts may also be manifested by complications such as infection, gastrointestinal bleeding, perforation, ulceration, fistula formation, obstruction, compression, or carcinoma arising in the cysts [7, 8]. Up to 10% of gastric duplications may contain ectopic pancreatic tissue which may lead to pancreatitis and mimic a pancreatic pseudocyst [3, 8].

Because of the rarity of adult gastric duplications, it is difficult to outline their natural history with certainty.

As with the native gastric mucosa, the cyst lining may undergo erosions, ulceration, and regenerative changes. In noncommunicating cysts, increased fluid production may result in pressure-induced necrosis of the mucosa. These changes may lead to bleeding into the cyst or perforation into the peritoneal cavity.

Duplication cysts have the potential for neoplastic transformation. The production of oncofetal antigens raises the problem of a precancerous condition in long standing intestinal duplications [8]. Out of 11 reported cases of malignancy arising within the duplication cysts, 8 were adenocarcinomas [4]. Five of the carcinomas originated from gastric duplications. Adenomyoma arising from a gastric duplication has also been reported [4]. Malignancies arising from duplication cysts are likely to be present at advanced stages because of their unusual symptoms and difficulty of diagnosis [4].

Although it is difficult to diagnose GDC preoperatively, recent imaging modalities have provided some informative findings. CT scan and endoscopic ultrasound (EUS) are the best ways to identify GDC [8]. Classically, radiographic studies show an intramural filling defect indenting the gastric contour [8]. Contrast-enhanced CT scan typically demonstrates GDC as a thick-walled cystic lesion with enhancement of the inner lining [2]. Calcification is occasionally observed on CT. These findings are of diagnostic significance for GDCs [2]. However, since mucinous cystic tumors of the pancreas also show similar radiological features, GDCs adjoining the pancreas are indistinguishable from pancreatic mucinous cystic tumors based on these CT findings. Moreover, because the wall is sometimes thin, enhancement of the inner cyst wall is not always demonstrated. Generally, MRI can provide additional information about the cyst content compared to CT scan. However, the nature of the fluid in the GDC was reported to differ in each case according to bleeding, chronic inflammation, or infection. Therefore, MRI seems to be of less significance than expected in diagnosing GDCs [2].

EUS is useful in distinguishing between the intramural and extramural lesions of the stomach. When EUS demonstrates a cyst with an echogenic internal mucosal layer and a hypoechoic intermediate muscular layer, the diagnosis of GDC is highly likely[2]. The role of EUS-guided FNA in GDC is uncertain because (a) the cytological features of GDC may closely resemble those of mucinous pancreatic neoplasms, and (b) GDCs with elevated levels of CEA and CA19-9 have been reported, mimicking mucinous pancreatic neoplasms [4, 8, 11].

Complete removal is the treatment choice to avoid the risk of possible complications such as obstruction, torsion, perforation, hemorrhage, and malignancy [9, 10]. A noncommunicating GDC is classically treated by complete excision of the cyst and resection of the shared wall between stomach and the duplication cyst [8]. Communicating GDC usually requires no intervention when both gastric lumens are patent [8]. Drainage and marsupialization of the cyst have been suggested. However, marsupialization into the stomach exposes the unprotected mucosa of the cyst to gastric contents with the risk of ulceration [4]. Drainage procedures such as cystojejunostomy may be complicated by stenosis of the anastomosis or blind loop syndrome and therefore discouraged [4]. Furthermore, leaving the cyst in place is ill-advised given the potential for malignant transformation [4].

Conclusion

In summary, this unusual developmental anomaly should be included in the differential diagnosis of cystic masses of the gastrointestinal tract, and the possibility of malignancy should also be considered. While the diagnosis of gastrointestinal tract duplications may be suggested by imaging studies, more often the correct diagnosis is not established prior to surgery. Due to the risk of malignant transformation and other complications, GDCs should be treated surgically by complete resection.



IBD and ULTRASOUND

 

Objectives—Transcutaneous bowel sonography is a nonionizing imaging modality used in inflammatory bowel disease. Although available in Europe, its uptake in North America has been limited. Since the accuracy of bowel sonography is highly operator dependent, low-volume centers in North America may not achieve the same diagnostic accuracy reported in the European literature. Our objective was to determine the diagnostic accuracy of bowel sonography in a nonexpert low-volume center.

Methods—All cases of bowel sonography at a single tertiary care center during an 18-month period were reviewed. Bowel sonography was compared with reference standards, including small-bowel follow-through, computed tomography, magnetic resonance imaging, colonoscopy, and surgical findings.

Results—A total of 103 cases were included for analysis during the study period. The final diagnoses included Crohn disease (72), ulcerative colitis (8), hemolytic uremic syndrome (1), and normal (22). The sensitivity and specificity of bowel sonography for intestinal wall inflammation were 87.8% and 92.6%, respectively. In the subset of patients who had complications of Crohn disease, the sensitivity and specificity were 50% and 100% for fistulas and 14% and 100% for strictures. One patient had an abscess, which was detected by bowel sonography. Abnormal bowel sonographic findings contributed to the escalation of treatment in 55% of cases.

Conclusions—Bowel sonography for inflammatory bowel disease can be performed in low-volume centers and provides diagnostic accuracy for luminal disease comparable with published data, although it is less sensitive for complications of Crohn disease.

 



DEEP PLANTAR FASCIA INJECTIONS

ULTRASOUND and DYSPERMIA

 

Abstract

Objectives—Sonography is a noninvasive, office-based diagnostic tool often used for evaluation of subfertile men. Previous studies have suggested that a resistive index (RI) greater than 0.6 is associated with impaired spermatogenesis. We sought to validate this threshold in a urologic patient population presenting for infertility evaluation.

Methods—We retrospectively reviewed 99 consecutive patients seen for nonobstructive male infertility at our institution. Patient demographics, semen analysis parameters, hormone profiles, lipid profiles, and penile and scrotal sonographic measurements were recorded. The RI was calculated from measurements of the peak systolic velocity and end-diastolic velocity. Ninety-one patients fit the inclusion criteria and were subsequently divided into 2 groups based on RI: group 1 with RI values of 0.6 or less (n = 49) and group 2 with RI values greater than 0.6 (n = 42).

Results—Variables that were significantly different between the groups included age, total sperm count, percent motile sperm, total motile sperm, follicle-stimulating hormone, high-density lipoprotein, and testis volume. On the other hand, body mass index, forward progression, World Health Organization score, total testosterone, free testosterone, estradiol, total cholesterol, low-density lipoprotein, and triglycerides were not significantly different between the groups. A receiver operating characteristic curve revealed an area under the curve of 0.64 (confidence interval, 0.52–0.75; P = .025). At the threshold of greater than 0.6, the RI had specificity of 63.27% and a 1.56 likelihood ratio to predict total motile sperm less than 20 × 10⁶ at spermatogenesis.

Conclusions—An intratesticular RI greater than 0.6 is associated with impaired spermatogenesis. This finding supports the use of testicular spectral Doppler sonography as a noninvasive tool for evaluation of testicular function

Discussion

The RI is calculated from measurements of the PSV and EDV. However, the PSV and EDV are dependent on the angle of incidence given by the Doppler formula. The Doppler angle is the angle of incidence between the ultrasound beam and the estimated flow direction. Doppler sonography accurately measures velocity (speed and direction of the movement) only at Doppler angles of 0° and 180°. Angles greater than 60° produce too large of an error in velocity and should not be used. Therefore, variation in the angle of incidence substantially influences the PSV and EDV. The RI, in contrast, is an angle- and operator-independent ratio, making it a reliable indicator. We used the average RI from both testes as an indicator, assuming that both testes contribute equally to semen parameters in spermatogenesis.

The standard RI of the testes was categorized in several animal studies. Carrillo et al11 examined 5 dogs over a 6-month period to determine that PSV, EDV, and RI measurements remained stable. Tarhan et al12 showed that the RI did not change in the contralateral artery after unilateral testicular torsion in a study of 24 canines, suggesting that unilateral testicular torsion does not alter contralateral testicular blood flow. Pozor and McDonnell13 evaluated 52 stallions to determine reference values for the PSV, EDV, and RI in nonpathogenic testes and found that obtaining the RI was feasible and that RI measurements for left and right testes were similar.

The testicular arterial RI has also has been studied for its predictive values in testicular disease. Jee et al14 studied the RI in scrotal inflammatory disease. They found that the RI could provide a diagnostic criterion for scrotal inflammatory disease if the values for the intratesticular and epididymal arteries were less than 0.5 and less than 0.7, respectively. Lefort et al15 studied the RI in 5 patients with testicular infarction caused by epididymo-orchitis. They found that an elevated RI can be suggestive of ischemia.

Further studies have examined the role of the RI in testicular microcirculation. Unsal et al16 examined RI values of 49 healthy patients. Fifteen were classified by sonography as having left-sided varicoceles and were compared to the other group of 34. The RI values were found to be significantly higher in the varicocele group compared to the control group (0.68 versus 0.64, respectively; P < .05).

The potential alteration of the RI in dyspermia has been investigated in 2 studies.5,6 Biagiotti et al5 assessed whether sonographic values such as the PSV, EDV, and RI may be useful in distinguishing the various causes of dyspermia compared to FSH and testicular volume. They recruited 161 patients: 9 with obstructive azoospermia, 20 with nonobstructive azoospermia, 17 with oligoasthenospermia, 38 with undetermined oligoasthenospermia, 19 with male accessory gland inflammation, 11 with clinical varicoceles, 32 with normal sperm analysis results plus recent paternity, and 15 with normal sperm analysis results plus recent paternity and varicoceles. They found that only the RI and PSV were correlated with the sperm production rate score, whereas FSH, testicular volume, and the EDV were not. In our study, we found that FSH does correlate with total motile sperm, whereas the PSV does not. The PSV is limited by its angle-dependent characteristic. Follicle-stimulating hormone has been shown to correlate with sperm production in previous studies.17,18

Pinggera et al6 also examined whether the RI can be used to predict dyspermia. They recruited 160 patients and divided them into 2 groups of 80. One group had mild oligoasthenozoospermia on semen analysis, whereas the control group had normal semen analysis results as well as paternity within 14 months of recruitment. The control group had a mean RI of 0.54 ± 0.05, whereas the cohort had a mean RI of 0.68 ± 0.06. The upper RI limit for a patient with normal semen analysis results was 0.6. They concluded that an RI greater than 0.6 may be indicative of a pathologic sperm count in urologic patients. Therefore, the objective in our study was to validate whether this conclusion was true in a urologic population presenting for a subfertility or infertility workup. We also sought to determine whether a lower RI threshold can be associated with impaired spermatogenesis.

When comparing the groups with an RI greater than 0.6 and an RI of 0.6 or less, we found a significant difference in total motile sperm (P < .01). This finding confirms the hypothesis by Pinggera et al6 that an RI greater than 0.6 is associated with dyspermia. Furthermore, we found that at an RI greater than 0.6, the sensitivity for total motile sperm less than 20 × 10⁶ was 57.14%, and specificity was 63.27%, with a 1.56 likelihood ratio. An RI of 0.56 or greater was also significantly associated with lower total motile sperm (P = .04). At that level, the sensitivity for total motile sperm less than 20 × 10⁶ was 69.05%, and specificity was 46.94%, with a likelihood ratio of 1.3.

Patients with obstructive azoospermia were excluded from the study, since we do not know the effect of tubal obstruction on the RI, and we wanted to examine the relationship between the RI and semen analysis. However, it was noted that in patients with nonobstructive azoospermia, the average Johnsen score was 2.5, and the average RI was 0.63. This RI was higher than the RI recorded for the excluded patients from our study who had obstructive azoospermia. Their collective average RI was 0.5, and their average Johnsen score was 10. Additional study is needed to determine whether this observation of a higher RI in nonobstructive azoospermia is valid, whether the RI varies in testes with nonobstructive azoospermia, and whether the RI can be used to identify localized pockets of spermatogenesis.

The explanation behind the association of testicular blood flow and spermatogenesis has yet to be fully elucidated. Testicular arteries are targets for androgens,19 and a study by Jezek et al20 showed that the testicular blood vessels in hyalinized human testes had an enlarged endothelial layer. More research is needed to clarify whether the impaired testicular microcirculation as reflected by an elevated RI is secondary to systemically impaired vascular functioning or a consequence of decreased testicular function.

A correlation of the RI with testicular biopsy is needed to state that an altered RI identifies spermatogenic dysfunction. Nonetheless, spectral Doppler analysis of the subfertile man has several present and potential clinical applications. Presently, available studies suggest that the RI should be used together with semen analysis and hormonal studies as part of the clinical evaluation of the subfertile man. It is a direct method of evaluating intratesticular blood flow and, as suggested by this and prior articles, yields reproducible data. Spectral Doppler sonography is a noninvasive technique that adds unique information about the intratesticular vasculature that can guide the physician in counseling the subfertile couple. Future studies will define the association of spectral Doppler findings and spermatogenesis as well as determine the spectral Doppler changes occurring with medical and/or surgical therapy and, by extension, spermatogenesis.

In conclusion, an intratesticular RI greater than 0.6 is associated with decreased total motile sperm, decreased testicular size, and increased FSH, supporting its use as an independent indicator of testicular function. Although further correlation with testis biopsy is needed, our data support the use of testicular sonography, and in particular spectral Doppler imaging, as a noninvasive tool for evaluation of testicular function in the subfertile man.

World Hepatitis Day 28 July

World Hepatitis Day, 28 July 2013

This is hepatitis. Know it. Confront it

Every year on 28 July, WHO and partners mark World Hepatitis Day to increase the awareness and understanding of viral hepatitis and the diseases that it causes.

Hepatitis viruses A, B, C, D and E can cause acute and chronic infection and inflammation of the liver that can lead to cirrhosis and liver cancer. These viruses constitute a major global health risk with around 240 million people being chronically infected with hepatitis B and around 150 million people chronically infected with hepatitis C.

For 2013, the overall theme continues to be "This is hepatitis. Know it. Confront it." The campaign emphasizes the fact that hepatitis remains largely unknown as a health threat in much of the world.

Goal: moving from awareness to commitment and action to address the "silent epidemic" of viral hepatitis

Millions of people are living with viral hepatitis and millions more are at risk of becoming infected. Most people with chronic infection with hepatitis B or C are unaware that they continue to carry the virus. They are therefore at high risk of developing severe chronic liver disease and can unknowingly transmit the virus to other people. Approximately one million people die each year from causes related to viral hepatitis, most commonly cirrhosis and liver cancer.

World Hepatitis Day provides an opportunity to focus on specific actions, such as:

·         strengthening prevention, screening and control of viral hepatitis and its related diseases;

·         increasing hepatitis B vaccine coverage and integration of the vaccine into national immunization programmes;

·         coordinating a global response to viral hepatitis.

Although the burden of disease related to hepatitis infection is very high, in most countries, the problem has not been addressed in a comprehensive way for many reasons. These include the fact that most people do not develop any symptoms when they become infected and that they remain free of symptoms often for decades until they develop chronic liver disease. This has largely resulted in "the silent epidemic" we are experiencing today.

Viral hepatitis also places a heavy burden on the health-care system because of the high costs of treatment of liver cancer and liver failure from cirrhosis. In many countries, liver failure from viral hepatitis is the leading reason for liver transplants. Such end-stage treatments are expensive, easily costing up to hundreds of thousands of dollars per person.

The date of 28 July was chosen for World Hepatitis Day in honour of the birthday of Nobel Laureate Professor Baruch Samuel Blumberg, discoverer of the hepatitis B virus.

Rosalind Franklin, "the woman who was not awarded the Nobel prize for the co-discovery of the structure of DNA".

Rosalind Franklin, DNA scientist, celebrated by Google doodle from guardian.co.uk,

British biophysicist and x-ray crystallographer helped discover DNA's structure but controversially missed out on Nobel prize


Thursday 25 July 2013 01.24 BST

The Google doodle dedicated to Rosalind Franklin. Photograph: Screen grab

The latest Google doodle celebrates the life and work of British biophysicist and x-ray crystallographer Rosalind Franklin, whose research led to the discovery of the structure of DNA.
Franklin was born in Notting Hill, London on 25 July 1920.
The second "o" in the doodle contains her image, while the "l" has been replaced with the DNA double helix.

Franklin also made critical contributions to our understanding of the molecular structures of RNA, viruses, coal and graphite.

She died from ovarian cancer in April 1958, aged just 37.

The scientist has perhaps become best known as "the woman who was not awarded the Nobel prize for the co-discovery of the structure of DNA".

During her DNA research, Franklin worked at King's College London under Maurice Wilkins.

The story goes that he took some of her x-ray crystallography images without her knowledge and showed them to his friends, Francis Crick and James Watson, who were also trying to discover the structure of DNA.

Wilkins, Crick and Watson were awarded the Nobel prize in Chemistry in 1962.

Crick later acknowledged that Franklin's images were "the data we actually used" to formulate their 1953 hypothesis regarding the structure of DNA.

The most significant of those images is known as Photo 51, which is also the inspiration for an exhibition currently at Somerset House in London.
________________________________

Photo 51 is the nickname given to an X-ray diffraction image of DNA taken by Raymond Gosling in May 1952 ^[1] under the direction of Rosalind Franklin^[2][3][4] at King's College London in Sir John Randall's group. It was critical evidence ^[5] in identifying the structure of DNA. ^[6]
James Watson was shown the photo by Maurice Wilkins, and along with Francis Crick, Watson used characteristics and features of Photo 51 to develop the chemical model of DNA molecule. In 1962, the Nobel Prize in Physiology or Medicine was awarded to Watson, Crick and Wilkins. The prize was not awarded to Franklin; she had died 4 years earlier, making her ineligible for nomination. ^[7]
The photograph provided key information that was essential for developing a model of DNA.^[8][9] The diffraction pattern determined the helical nature of the double helix strands (antiparallel). The outside linings of DNA have a phosphate backbone, and codes for inheritance are inside the helix. Watson and Crick's calculations from Franklin's photography gave crucial parameters for the size and structure of the helix. ^[8][10][11]
Photo 51 became a crucial data source^[12] that led to the development of the DNA model and confirmed the prior postulated double helical structure of DNA, which were presented in the articles in the Nature journal by Raymond Gosling.

As historians of science have re-examined the period during which this image was obtained, considerable controversy has arisen over both the significance of the contribution of this image to the work of Watson and Crick, as well as the methods by which they obtained the image. Franklin was hired independently of Maurice Wilkins, who, nonetheless, showed Photo 51 to Watson and Crick, without her knowledge. Whether Franklin would have deduced the structure of DNA on her own, from her own data, had Watson and Crick not obtained her image, is a hotly debated topic,^[13][14][15] made more controversial by the negative caricature of Franklin presented in Watson's history of the research on DNA structure, The Double Helix.^[13][16][17] Watson later admitted his distortion of Franklin in his book, noting in a preface to a later edition: "Since my initial impressions about [Franklin], both scientific and personal (as recorded in the early pages of this book) were often wrong, I want to say something here about her achievements." 
[From Wikipedia]
_____________________________

Rosalind Franklin biography

Born On This Day

Rosalind Franklin was born on this day in 1920.

 

Quick Facts

• NAME: Rosalind Franklin
• OCCUPATION:Chemist
• BIRTH DATE:July 25, 1920
• DEATH DATE:April 16, 1958
• EDUCATION: Newnham College, Cambridge University
• PLACE OF BIRTH: London, England
• PLACE OF DEATH: London, England
• Full Name: Rosalind Elsie Franklin
• AKA: Rosalind Franklin

Best Known For

British chemist Rosalind Franklin is best known for her role in the discovery of the structure of DNA ,and for her pioneering use of X-ray diffraction.

---

Synopsis

Born in 1920 in London, Rosalind Franklin earned a Ph.D. in physical chemistry from Cambridge University. She learned crystallography and X-ray diffraction, techniques that she applied to DNA fibers. One of her photographs provided key insights into DNA structure. Other scientists used it as the basis for their DNA model and took credit for the discovery. Franklin died of ovarian cancer in 1958, at age 37.

Early Years

British chemist Rosalind Elsie Franklin was born into an affluent and influential Jewish family on July 25, 1920, in Notting Hill, London, England. She displayed exceptional intelligence from early childhood, knowing from the age of 15 that she wanted to be a scientist. She received her education at several schools, including North London Collegiate School, where she excelled in science, among other things.

Rosalind Franklin enrolled at Newnham College, Cambridge, in 1938 and studied chemistry. In 1941, she was awarded Second Class Honors in her finals, which, at that time, was accepted as a bachelor's degree in the qualifications for employment. She went on to work as an assistant research officer at the British Coal Utilisation Research Association, where she studied the porosity of coal—work that was the basis of her 1945 Ph.D. thesis "The physical chemistry of solid organic colloids with special reference to coal."

In the fall of 1946, Franklin was appointed at the Laboratoire Central des Services Chimiques de l'Etat in Paris, where she worked with crystallographer Jacques Mering. He taught her X-ray diffraction, which would largely play into her discovery of "the secret of life"—the structure of DNA. In addition, Franklin pioneered the use of X-rays to create images of crystalized solids in analyzing complex, unorganized matter, not just single crystals.

Scientific Discoveries and Credit Controversy

In January 1951, Franklin began working as a research associate at the King's College London in the biophysics unit, where director John Randall used her expertise and X-ray diffraction techniques (mostly of proteins and lipids in solution) on DNA fibers. Studying DNA structure with X-ray diffraction, Franklin and her student Raymond Gosling made an amazing discovery: They took pictures of DNA and discovered that there were two forms of it, a dry "A" form and a wet "B" form. One of their X-ray diffraction pictures of the "B" form of DNA, known as Photograph 51, became famous as critical evidence in identifying the structure of DNA. The photo was acquired through 100 hours of X-ray exposure from a machine Franklin herself had refined.

John Desmond Bernal, one of the United Kingdom’s most well-known and controversial scientists and a pioneer in X-ray crystallography, spoke highly of Franklin around the time of her death in 1958. "As a scientist Miss Franklin was distinguished by extreme clarity and perfection in everything she undertook," he said. "Her photographs were among the most beautiful X-ray photographs of any substance ever taken. Their excellence was the fruit of extreme care in preparation and mounting of the specimens as well as in the taking of the photographs."

 

Despite her cautious and diligent work ethic, Franklin had a personality conflict with colleague Maurice Wilkins, one that would end up costing her greatly. In January 1953, Wilkins changed the course of DNA history by disclosing without Franklin's permission or knowledge her Photo 51 to competing scientist James Watson, who was working on his own DNA model with Francis Crick at Cambridge.

Upon seeing the photograph, Watson said,

"My jaw fell open and my pulse began to race," according to author Brenda Maddox, who in 2002 wrote a book about Franklin titled Rosalind Franklin: The Dark Lady of DNA.

The two scientists did in fact use what they saw in Photo 51 as the basis for their famous model of DNA, which they published on March 7, 1953, and for which they received a Nobel Prize in 1962. Crick and Watson were also able to take most of the credit for the finding: When publishing their model in Nature magazine in April 1953, they included a footnote acknowledging that they were "stimulated by a general knowledge" of Franklin's and Wilkins' unpublished contribution, when in fact, much of their work was rooted in Franklin's photo and findings. Randall and the Cambridge laboratory director came to an agreement, and both Wilkins' and Franklin's articles were published second and third in the same issue of Nature. Still, it appeared that their articles were merely supporting Crick and Watson's.

According to Maddox, Franklin didn't know that these men based their Nature article on her research, and she didn't complain either, likely as a result of her upbringing. Franklin "didn't do anything that would invite criticism … [that was] bred into her," Maddox was quoted as saying in an October 2002 NPR interview.

Franklin left King's College in March 1953 and relocated to Birkbeck College, where she studied the structure of the tobacco mosaic virus and the structure of RNA. Because Randall let Franklin leave on the condition that she would not work on DNA, she turned her attention back to studies of coal. In five years, Franklin published 17 papers on viruses, and her group laid the foundations for structural virology.

Illness and Death

In the fall of 1956, Franklin discovered that she had ovarian cancer. She continued working throughout the following two years, despite having three operations and experimental chemotherapy. She experienced a 10-month remission and worked up until several weeks before her death on April 16, 1958, at the age of 37.

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