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The Bahrain Medical Bulletin published an article titled "Talent in Medicine" by Dr. Anil Kumar Chawla. The article discusses how individuals in the medical profession have diverse talents and interests outside of medicine, such as music, art, writing, and sports. It also mentions that some medical professionals apply their knowledge to fields like clinical practice, pharmacology, and folk medicine. The article includes two poems titled "Why?" and "Zero is Hero!" and invites contributors to submit their literary works. This issue of the bulletin also commemorates 25 years since Dr. Chawla's poems were first published in the journal. [Extracted from the article]

The medical profession is not different from other workforce, sharing common interests, hobbies and talents. The majority of these activities are unrelated to medicine. Many are musicians, performers, artists, writers, critics, astronomers, photographers, etc., not to mention their excellence in the world of sports. On the other hand, there are also instances when the practice of these activities takes the form of applied interpretation of what they know in human pathobiology and the concerned function. Thus, some may be historians of clinical practice, clinical pharmacologists of locally used herbs or clinical therapists of locally practiced folk medicine. This section of the Bahrain Medical Bulletin will be devoted to "Talents in the Medical Profession" to show and exchange with others common interests and applied experience. Contributors are therefore welcomed to submit their literary works. [ABSTRACT FROM AUTHOR]

Background & objectives: Cervical cancer is a major health problem and a leading cause of death among women in India. Of all the associated risk factors, high-risk human papillomavirus (HPV) infections being the principal aetiologic agent, two HPV vaccines are in use for the control of cervical cancer. The present study was undertaken to explore the knowledge, attitude and practice (KAP) on HPV vaccination among the healthcare providers in India. Methods: A cross-sectional study was conducted among 590 healthcare professionals from 232 hospitals and 80 PHCs of nine districts of Delhi-NCR (National Capital Region). A total of 590 (526 female, 64 male) healthcare providers were surveyed. Results: Only 47 per cent of respondents recommended young women to get vaccinated against HPV. Majority of respondents (81%) were found to be aware about the existence of vaccines for cervical cancer prevention. District-wise, highest (88.3%) awareness about the existence of vaccines against HPV was reported from Gautam Budh Nagar and lowest (64%) in Faridabad. Although 86 per cent of gynaecologists were aware about the names of HPV vaccines available in the market, only 27 per cent of paramedical staff had this knowledge. There was a significant difference between the respondents from government and private sectors regarding their awareness about HPV vaccines. Lack of awareness about the principal cause, risk factors and symptoms for cervical cancer and HPV vaccination was significantly (P<0.05) reported in the respondents from paramedical staff category. Interpretation & conclusions: The findings reinforce continued medical education of healthcare providers, particularly those from the government sector on HPV vaccination for cervical cancer prevention. Public education is also pertinent for a successful HPV vaccination programme in the country. [ABSTRACT FROM AUTHOR]

The medical profession is not different from other workforce, sharing common interests, hobbies and talents. The majority of these activities are unrelated to medicine. Many are musicians, performers, artists, writers, critics, astronomers, photographers, etc., not to mention their excellence in the world of sports. On the other hand, there are also instances when the practice of these activities takes the form of applied interpretation of what they know in human pathobiology and the concerned function. Thus, some may be historians of clinical practice, clinical pharmacologists of locally used herbs or clinical therapists of locally practiced folk medicine. This section of the Bahrain Medical Bulletin will be devoted to "Talents in the Medical Profession" to show and exchange with others common interests and applied experience. Contributors are therefore welcomed to submit their literary works. This issue contains two poems titled "Get off the train!" and "T for tolerance!". [ABSTRACT FROM AUTHOR]

The medical profession is not different from other workforce, sharing common interests, hobbies and talents. The majority of these activities are unrelated to medicine. Many are musicians, performers, artists, writers, critics, astronomers, photographers, etc., not to mention their excellence in the world of sports. On the other hand, there are also instances when the practice of these activities takes the form of applied interpretation of what they know in human pathobiology and the concerned function. Thus, some may be historians of clinical practice, clinical pharmacologists of locally used herbs or clinical therapists of locally practiced folk medicine. This section of the Bahrain Medical Bulletin will be devoted to "Talents in the Medical Profession" to show and exchange with others common interests and applied experience. Contributors are therefore welcomed to submit their literary works. This issue contains two poems titled "My Life boat!" and "The blind doctors!". [ABSTRACT FROM AUTHOR]

Examines the role of transforming growth factor-beta (TGFβ) receptor with endosomal protein EEA1 in signaling to Smad2. Importance of TGFβ in cellular growth; Internalization of TGFβ receptor; Derivation of TGFβ signaling.

The medical profession is not different from other workforce, sharing common interests, hobbies and talents. The majority of these activities are unrelated to medicine. Many are musicians, performers, artists, writers, critics, astronomers, photographers, etc., not to mention their excellence in the world of sports. On the other hand, there are also instances when the practice of these activities takes the form of applied interpretation of what they know in human pathobiology and the concerned function. Thus, some may be historians of clinical practice, clinical pharmacologists of locally used herbs or clinical therapists of locally practiced folk medicine. This section of the Bahrain Medical Bulletin will be devoted to “Talents in the Medical Profession” to show and exchange with others common interests and applied experience. Contributors are therefore welcomed to submit their literary works. This issue contains two poems titled “Adam and Eve!” and “Hats Off!” [ABSTRACT FROM AUTHOR]

Identifies possible structural elements in the glucose transporter (GLUT4) and transporter isoform (GLUT1) proteins that determine their cellular localization. Cell culture; Construction of HA-tagged chimera transporters; Transient expression of HA-epitope-tagged chimera transporter cDNA in COS-7 cells; Immunofluorescence of transfected cells.

The medical profession is not different from other workforce, sharing common interests, hobbies and talents. The majority of these activities are unrelated to medicine. Many are musicians, performers, artists, writers, critics, astronomers, photographers, etc., not to mention their excellence in the world of sports. On the other hand, there are also instances when the practice of these activities takes the form of applied interpretation of what they know in human pathobiology and the concerned function. Thus, some may be historians of clinical practice, clinical pharmacologists of locally used herbs or clinical therapists of locally practiced folk medicine. This section of the Bahrain Medical Bulletin will be devoted to "Talents in the Medical Profession" to show and exchange with others common interests and applied experience. Contributors are therefore welcomed to submit their literary works. This issue contains two poems titled "I Want Peace!" and "M.I.N.D.". [ABSTRACT FROM AUTHOR]

The poem "What's Happening?" by Anil Kumar is presented. First Line: When a 'yawn' or 'sneeze' comes, it comes; you can't stop it, Last Line: You allow or change what happens; don't stress over what happens!

Two poems by Anil Kumar Chawla are presented. "Our Sorrows." First Line: Man or woman, we've all encountered sorrow, Last Line: When I wear correct thinking glasses, distortion goes there is no sorrow. "Ground Zero." First Line: We are so impressed by levels of men and women - some dull some glow, Last Line: This world will be heaven we won't have to die to reach heaven's shores.

An introduction is presented in which the editor discusses various topics within the issue including the poems "Retired? Now Unlearn!," "Living as Being!," and the talents in medical professionals.

The poem "It's Only Memory Dear" is presented. First Line: It's only your memory, dear! Last Line: You may live every days's every moment lightly, joyfully.

The poem "The 'I' Bug" is presented. First Line: Bugs of all kinds, you know, bite and cause disease, Last Line: 'I' bug.

Two poems by Anil Chawla are presented. "Home." First Line: Home is where you come back and find rest, Last Line: It brings love and joy that emanates from this silence. "The Goalkeeper." First Line: When you were born, you didn't know a word, Last Line: restored within.

Two poems by Anil Kumar Chawla are presented. "I Love You!." First Line: I told her �I love you', you're beautiful, Last Line: I'm still lost; what do you say? What's the answer to this riddle? "Be Real!." First Line: What is non- existent now is unreal, Last Line: This moment is real, to be real live fully in this moment.

Two poems by Anil Kumar Chawla is presented. "Who Is He?" First Line: I am not what I keep telling myself who I am, Last Line: Do keep the possibility, infinity may have come to the shore! "Walk, Don't Run!" First Line: Walk, don't run! is a Hollywood movie of the seventies?, Last Line: As the body walked, my mind rested in its saddle.

Two poems by Dr. Anil Kumar Chawla are presented. "Bathing Oneself." First Line: 'Take a bath daily' you were told when you were a child, Last Line: You wash yourself every moment; be centered every moment; smell like a fresh cake. "Sometimes." First Line: Sometimes You slow; Last Line: You won't forget the Being till the end of your earthly sojourn.

The poem "The Club Sixty" by Anil Kumar Chawla is presented. First Line: Happy birthday, so you are sixty now! Last Line: If you go with the flow, you'll live in happiness.

Two poems by Anil Kumar Chawla are presented. ''The War Within.'' First Line: I am at no war, not with anyone; Last Line: Not getting lost in automatic thoughts, that's the fight. ''The Silence Within.'' First Line: There is a core within you where silence reigns; Last Line: Through this inner silence, you access a realm of peace.

Two poems by Anil Kumar Chawla are presented. "Mindfulness to Mindlessness." First Line: Being mindful means to be aware! Last Line: restlessness. "The Missing Rider." First Line: There was a coach with five horses I saw in my dream, Last Line: A peaceful , calm ride is dawning on me, the coach is now my convenience!

The liver is a major site of glucose, fatty acid, and triglyceride (TG) synthesis and serves as a major regulator of whole body nutrient homeostasis. Chronic exposure of humans or rodents to high-calorie diets promotes non-alcoholic fatty liver disease, characterized by neutral lipid accumulation in lipid droplets (LD) of hepatocytes. Here we show that the LD protein hypoxia-inducible gene 2 (Hig2/Hilpda) functions to enhance lipid accumulation in hepatocytes by attenuating TG hydrolysis. Hig2 expression increased in livers of mice on a high-fat diet and during fasting, two states associated with enhanced hepatic TG content. Hig2 expressed in primary mouse hepatocytes localized to LDs and promoted LD TG deposition in the presence of oleate. Conversely, tamoxifen-inducible Hig2 deletion reduced both TG content and LD size in primary hepatocytes from mice harboring floxed alleles of Hig2 and a cre/ERT2 transgene controlled by the ubiquitin C promoter. Hepatic TG was also decreased by liver-specific deletion of Hig2 in mice with floxed Hig2 expressing cre controlled by the albumin promoter. Importantly, we demonstrate that Hig2-deficient hepatocytes exhibit increased TG lipolysis, TG turnover, and fatty acid oxidation as compared with controls. Interestingly, mice with liver-specific Hig2 deletion also display improved glucose tolerance. Taken together, these data indicate that Hig2 plays a major role in promoting lipid sequestration within LDs in mouse hepatocytes through a mechanism that impairs TG degradation. [ABSTRACT FROM AUTHOR]

Myoblast differentiation into mature myotubes is a critical step in the development and repair of human skeletal muscle. Here we show that small interfering RNA (siRNA)-based silencing of the Ste20-like mitogen-activated protein 4 kinase 4 (Map4k4) in C2C12 myoblasts markedly enhances expression of myogenic differentiation genes, myoblast fusion, and myotube diameter. In contrast, adenovirus-mediated expression of native Map4k4 in C2C12 cells attenuates each of these processes, indicating that Map4k4 is a negative regulator of myogenic differentiation and hypertrophy. Expression of a Map4k4 kinase-inactive mutant enhances myotube formation, suggesting that the kinase activity of Map4k4 is essential for its inhibition of muscle differentiation. Map4k4 regulation of myogenesis is unlikely to be mediated by classic mitogen-activated protein kinase (MAPK) signaling pathways, because no significant difference in phosphorylation of extracellular signal-regulated kinase (ERK), p38, or c-Jun N-terminal kinase (JNK) is observed in Map4k4-silenced cells. Furthermore, silencing of these other MAPKs does not result in a hypertrophic myotube phenotype like that seen with Map4k4 depletion. Uniquely, Map4k4 silencing upregulates the expression of the myogenic regulatory factor Myf5, whose depletion inhibits myogenesis. Furthermore, Myf5 is required for enhancement of myotube formation in Map4k4-silenced cells, while Myf5 overexpression rescues Map4k4-mediated inhibition of myogenic differentiation. These results demonstrate that Map4k4 is a novel suppressor of skeletal muscle differentiation, acting through a Myf5-dependent mechanism. [ABSTRACT FROM AUTHOR]

Protein kinase B/Akt protein kinases control an array diverse functions, including cell growth, survival, proliferation, and metabolism. We report here the identification of pleckstrin homology-like domain family B member 1 (PHLDB1) as an insulin-responsive protein that enhances Akt activation. PHLDB1 contains a pleckstrin homology domain, which we show phosphatidylinositol PI(3,4)P2, PI(3,5)P2, and PI(3,4,5)P3, well as a Forkhead-associated domain and coiled coil regions. PHLDB1 expression is increased during adipocyte differentiation, and it is abundant in many mouse tissues. Both endogenous and HA- or GFP-tagged PHLDB1 displayed a cytoplasmic disposition in unstimulated cultured adipocytes but translocated to the plasma membrane in response to insulin. Depletion of PHLDB1 by siRNA inhibited insulin stimulation of phosphorylation but not tyrosine phosphorylation of IRS-RNAi-based silencing of PHLDB1 in cultured adipocytes attenuated insulin-stimulated deoxyglucose transport Myc-GLUT4-EGFP translocation to the plasma membrane, whereas knockdown of the PHLDB1 isoform PHLDB2 failed attenuate insulin-stimulated deoxyglucose transport. Furthermore, adenovirus-mediated expression of PHLDB1 in adipocytes enhanced insulin-stimulated Akt and p70 S6 kinase phosphorylation, as well as GLUT4 translocation. These results indicate that PHLDB1 is a novel modulator of Akt protein kinase activation by insulin. [ABSTRACT FROM AUTHOR]

The receptor peroxisome proliferator-activated receptor γ (PPARγ) is considered a master regulator of adipocyte differentiation and promotes glucose and lipid metabolism in mature adipocytes. We recently identified the yeast Sterile 20 (Ste20) protein kinase ortholog, Map4k4, in an RNA interference-based screen as an inhibitor of PPARγ expression in cultured adipocytes. Here, we show that RNA interference-mediated silencing of Map4k4 elevates the levels of both PPAR'γ1 and PPARγ2 proteins in 3T3-L1 adipocytes without affecting PPARγ mRNA levels, suggesting that Map4k4 regulates PPARγ at a post-transcriptional step. PPARγ degradation rates are remarkably rapid as measured in the presence of cycloheximide (t½ = 2 h), but silencing Map4k4 had no effect on PPARγ degradation. However, depletion of Map4k4 significantly enhances [35S]methionine/cysteine incorporation into proteins, suggesting that Map4k4 signaling decreases protein translation. We show a function of Map4k4 is to inhibit rapamycin-sensitive mamma- Jian target of rapamycin (mTOR) activity, decreasing AE-BP1 phosphorylation. In addition, our results show mTOR and 4E-BP1 are required for the increased PPARγ protein expression upon Map4k4 knockdown. Consistent with this concept, adenovirus-mediated expression of Map4k4 decreased PPARγ protein levels and mTOR phosphorylation. These data show that Map4k4 negatively regulates PPARγ post-transcriptionally, by attenuating mTOR signaling and a 4E-BP 1-dependent mechanism. [ABSTRACT FROM AUTHOR]

Storage of energy as triglyceride in large adipose-specific lipid droplets is a fundamental need in all mammals. Efficient sequestration of fat in adipocytes also prevents fatty acid overload in skeletal muscle and liver, which can impair insulin signaling. Here we report that the Cide domain-containing protein Cidea, previously thought to be a mitochondrial protein, colocalizes around lipid droplets with perilipin, a regulator of lipolysis. Cidea-GFP greatly enhances lipid droplet size when ectopically expressed in preadipocytes or COS cells. These results explain previous findings showing that depletion of Cidea with RNAi markedly elevates lipolysis in human adipocytes. Like perilipin, Cidea and the related lipid droplet protein Cidec/FSP27 are controlled by peroxisome proliferator-activated receptor γ (PPARγ). Treatment of lean or obese mice with the PPARγ agonist rosiglitazone markedly up-regulates Cidea expression in white adipose tissue (WAT), increasing lipid deposition. Strikingly, in both omental and s.c. WAT from BMI-matched obese humans, expression of Cidea, Cidec/FSP27, and perilipin correlates positively with insulin sensitivity (HOMA-IR index). Thus. Cidea and other lipid droplet proteins define a novel, highly regulated pathway of triglyceride deposition in human WAT. The data support a model whereby failure of this pathway results in ectopic lipid accumulation, insulin resistance, and its associated comorbidities in humans. [ABSTRACT FROM AUTHOR]

Fat-specific protein (FSP)27/Cidec is most highly expressed in white and brown adipose tissues and increases in abundance by over 50-fold during adipogenesis. However, its function in adipocytes has remained elusive since its discovery over 15 years ago. Here we demonstrate that FSP27/Cidec localizes to lipid droplets in cultured adipocytes and functions to promote lipid accumulation. Ectopically expressed FSP27-GFP surrounds lipid droplets in 3T3-L1 adipocytes and colocalizes with the known lipid droplet protein perilipin. Immunostaining of endogenous FSP27 in 3T3-L1 adipocytes also confirmed its presence on lipid droplets. FSP27-GFP expression also mark- edly increases lipid droplet size and enhances accumulation of total neutral lipids in 3T3-L1 preadipocytes as well as other cell types such as COS cells. Conversely, RNA interference-based FSP27/Cidec depletion in mature adipocytes significantly stimulates lipolysis and reduces the size of lipid droplets. These data reveal FSP27/Cidec as a novel adipocyte lipid droplet protein that negatively regulates lipolysis and promotes triglyceride accumulation. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor α (TNFα) is a cytokine secreted by macrophages and adipocytes that contributes to the low grade inflammation and insulin resistance observed in obesity. TNFα signaling decreases peroxisome proliferator-activated receptor γ and glucose transporter isoform 4 (GLUT4) expression in adipocytes, impairing insulin action, and this is mediated in part by the yeast Ste20 protein kinase ortholog Map4k4. Here we show that Map4k4 expression is selectively up-regulated by TNFα, whereas the expression of the protein kinases JNK1/2, ERK1/2, p38 stress-activated protein kinase, and mitogen-activated protein kinase kinases 4/7 shows little or no response. Furthermore, the cytokines interleukin 1β (IL-1β) and IL-6 as well as lipopolysaccharide fail to increase Map4k4 mRNA levels in cultured adipocytes under conditions where TNFα elicits a 3-fold effect. Using agonistic and antagonistic antibodies and small interfering RNA (siRNA) against TNFα receptor 1 (TNFR1) and TNFα receptor 2 (TNFR2), we show that TNFR1, but not TNFR2, mediates the increase in Map4k4 expression. TNFR1, but not TNFR2, also mediates a potent effect of TNFα on the phosphorylation of JNK1/2 and p38 stress-activated protein kinase and their downstream transcription factor substrates c-Jun and activating transcription factor 2 (ATF2). siRNA-based depletion of c-Jun and ATF2 attenuated TNFα action on Map4k4 mRNA expression. Consistent with this concept, the phosphorylation of ATF2 along with the expression and phosphorylation of c-Jun by TNFα signaling was more robust and prolonged compared with that of IL-1β, which failed to modulate Map4k4. These data reveal that TNFα selectively stimulates the expression of a key component of its own signaling pathway, Map4k4, through a TNFR1-dependent mechanism that targets the transcription factors c-Jun and ATF2. [ABSTRACT FROM AUTHOR]

Glucose homeostasis is controlled in part by regulation of glucose uptake into muscle and adipose tissue. Intracellular membrane vesicles containing the GLUT4 glucose transporter move towards the cell cortex in response to insulin and then fuse with the plasma membrane. Here we show that the fusion step is retarded by the inhibition of phosphatidylinositol (PI) 3-kinase. Treatment of insulin-stimulated 3T3-L1 adipocytes with the PI 3-kinase inhibitor LY294002 causes the accumulation of GLUT4-containing vesicles just beneath the cell surface. This accumulation of GLUT4-containing vesicles near the plasma membrane prior to fusion requires an intact cytoskeletal network and the unconventional myosin motor Myo1c. Remarkably, enhanced Myo1c expression under these conditions causes extensive membrane ruffling and overrides the block in membrane fusion caused by LY294002, restoring the display of GLUT4 on the cell exterior. Ultrafast microscopic analysis revealed that insulin treatment leads to the mobilization of GLUT4-containing vesicles to these regions of Myo1c-induced membrane ruffles. Thus, localized membrane remodeling driven by the Myo1c motor appears to facilitate the fusion of exocytic GLUT4-containing vesicles with the adipocyte plasma membrane. [ABSTRACT FROM AUTHOR]

Insulin stimulates glucose uptake in muscle and adipose cells by mobilizing intracellular membrane vesicles containing GLUT4 glucose transporter proteins to the plasma membrane. Here we show in live cultured adipocytes that intracellular membranes co [ABSTRACT FROM AUTHOR]