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Jaspal S. Sandhu PhD

Assistant Adjunct Professor, Community Health Sciences

https://publichealth.berkeley.edu/people/jaspal-sandhu/

Your mouth is alive with living organisms bacteria which live and thrive in its warm hdrs depression test cheap zyban 150 mg mastercard, dark environment mood disorder management chart discount zyban 150 mg overnight delivery. Tere are literally more bacteria alive in your mouth right now than there are people on planet Earth or germs in a toilet bowl anxiety attack zyban 150mg with visa. Some of these bacteria are benefcial anxiety zone ms order zyban visa, helping your body to resist invaders and digest proteins. Other bacteria may be hostile, eventually resulting in things like sore throat or ear infection. Regardless of their intent, bacteria live and multiply in your mouth, below the surface of your tongue, at the back of your throat and on your tonsils (if you still have them) by the billions. Billions of bacteria eating and then secreting waste can result in a lot of foul-smelling material. Certain types of anaerobic, sulphur-producing-bacteria emit noxious smelling waste composed of volatile sulphur compounds. Tese compounds include hydrogen sulphide (smells like rotten eggs), methyl mercaptan (smells like rotten cabbage), putrescine and cadaverine (both smell like decay) and several other unpleasant odours. Some of these waste compounds are so potent they are also found in nature in the glands of skunks. The pungent smells that come from the waste of this type of bacteria are what we typically refer to as bad breath. Germs cause bad breath Bad breath is the result of billions of bad-breath-related bacteria eating left over proteins in your mouth and converting them to smelly, sulphur based waste. Anyone can get bad breath – even people who are conscientious brushers and fossers. It has less to do with oral hygiene and more to do with things like foods you eat, medications you take and personal habits you have that can provide an environment favorable to anaerobic, sul phur producing, bad-breath-related bacteria. Sometimes those natural defenses are insufficient to effectively limit bacteria colonies. This is when even someone with great oral hygiene habits can quickly begin to smell ofensive. Gum disease Diseased gum tissue feeds and harbors bacteria and provides opportunities for them to enter the bloodstream. Drying agents in Alcohol in mouthwash and detergents like Sodium Lauryl Sulphate in oral care products toothpaste can cause dry mouth. Sweets Sugars (sucrose, glucose, fructose) are efficient fuel for all types of bacteria ranging from bad-breath-related bacteria to the germs that are responsible for plaque, gum disease and tooth staining. Sugars also encourage tooth decay which feeds bacteria further and exacerbates bad breath problems. Everyone in the world has the same types of bacteria in their mouth (though they have them at diferent levels. You cannot and should not get rid of the bad breath related bacteria from your mouth entirely. Anaerobic sulphur-producing bacteria are part of our normal oral fora and are well established in a typical, healthy mouth. It is not possible to remove them permanently by tongue scraping, antibiotics, or harsh germ-fghting mouthwash. In addition, as they help your body in various functions like digestion of proteins, removing the bacteria is not recommended. They prefer to grow and multiply in the spaces in between the papillae (fbers) that make up your tongue, at the back of your throat and on your tonsils if you still have them. On the other hand, when your mouth is dry, bacteria populations grow very rapidly. It is possible to eliminate the smells associated with bad breath related bacteria by converting them to non-odourous organic salts without stripping the mouth of the bacterias protective benefts. The same bacteria that cause bad breath also help you to digest proteins and fght of hostile germs. Teir population and ability to metabolize waste needs to be controlled through an easy to use oral care regimen. Study continues into why diferent people have diferent levels of oral cavity bacteria populations. Teories attribute increases in bacteria populations to hormonal changes, dry mouth, illness, medications, etc. Any event that creates an imbalance in your oral fora can radically change the overall bacteria populations in your mouth. Higher populations of bad-breath-related bacteria leads to stronger and more frequent breath odour problems. Certain physical traits can predispose you to bad breath as they create an environment more favorable for bacteria. A rough tongue surface, fssures on your tongue, having tonsils, dental pockets or cavities can all provide shelter for bacteria that can then rapidly multiply. Bad breath is typically the result of an overabundance of bad-breath-related bacteria below the surface of your tongue and at the back of your throat. If you are brushing conscientiously and still get bad breath, you are probably just using the wrong toothpaste. Some toothpastes contain sodium lauryl sulphate, a soapy detergent that creates foam but has no cleaning beneﬁt. The additive has recently been linked to serious side effects including canker sores. Read the label of your toothpaste and avoid sodium lauryl sulphate as an ingredient. Katz Product Tip: Works faster and longer the Breath Co Toothpaste and the Breath Co Oral Rinse were developed speciﬁcally to ﬁght breath odour. Independent clinical trials have veriﬁed that nothing works faster or lasts longer to stop bad breath than the Breath Company products. The burning you feel comes from alcohol in the mouthwash irritating the inside of your mouth. Your mouth is supposed to be a moist place and alcohol rapidly dries and irritates it. Recent research published in The Australian Dental Journal has recently shown a potential link between alcohol-based mouthwash and oral cancer. There is as much alcohol in a capful of typical mouthwash as there is in a shot of vodka. It is possible to fail a police Breathalyzer test after rinsing with a mouthwash like Listerine. Katz Product Tip: No alcohol in our products the Breath Co Oral Rinse is alcohol-free and works without burning. Instead of an alcohol astringent, we use the power of oxygen to attack bad-breath-related bacteria and the odours they cause. Bad-breath-related bacteria live and breed within the back of the tongue and in the throat. Post-nasal drip, respiratory infection, and other conditions that allow protein-rich mucus to reach the back of the throat will provide food to the bacteria. The bacteria will then break down the protein in mucus and create volatile sulphur compounds resulting in bad breath and unpleasant mouth tastes. You may smell odour coming out of your nose, but the source is typically the back of the throat. Tere is no open tube connecting the large intestine, small intestine and stomach to your oesophagus and your mouth. Tere are valves, muscles, sphincters and so on that keep digested food in its proper place. If you burp or belch you may release smelly digestive gas but that is not bad breath. Parsley doesnt work Breath Assure was an oral care manufacturer in the 1990s that claimed that swallowing their parsley oil capsules could freshen breath from the inside out. Its a process called acclimation which we have developed over centuries of evolution – it helps us to be able to distinguish strange smells quickly without being overwhelmed with our own particular odours. You breathe your own breath constantly so you become accustomed to your own smell. Blow all day and you may not smell a thing even as people are backing away from you slowly. Dont waste your breath It is impossible to smell your own breath by exhaling into your cupped hand and then trying to smell the result. If you notice a yellowish stain where you wiped its likely that you have an elevated sulphide production level and potentially pungent breath.

S2 in the Supplementary were signif icant differences between these groups Appendix facebook depression definition discount zyban 150 mg line. As compared with participants who and the control group in 12 of the 14 items at remained in the trial depression definition dsm iv tr order cheap zyban on line, those who dropped out 3 years (Table S5 in the Supplementary Appen n engl j med 368;14 nejm depression test given by doctors buy discount zyban 150 mg online. Changes in objective biomarkers also indi nificantly increased their consumption of extra cated good compliance with the dietary assign virgin olive oil (to 50 and 32 g per day depression symptoms explained zyban 150mg, respec ments (Fig. The main nutrient changes in the Participants in the two Mediterranean-diet Mediterranean-diet groups reflected the fat con groups significantly increased weekly servings of tent and composition of the supplemental foods fish (by 0. No relevant diet-related adverse effects group (Table S6 in the Supplementary Appendix. We did not find any significant difference ranean diet with extra-virgin olive oil and those in changes in physical activity among the three assigned to a Mediterranean diet with nuts sig groups. A ponents of the primary end point, only the com total of 288 primary-outcome events occurred: parisons of stroke risk reached statistical signifi 96 in the group assigned to a Mediterranean diet cance (Table 3, and Fig. The Kaplan–Meier curves for the assigned to a Mediterranean diet with nuts primary end point diverged soon after the trial (3. Tak started, but no effect on all-cause mortality was ing into account the small differences in the ac apparent (Fig. The results of several sensitiv crual of person-years among the three groups, ity analyses were also consistent with the find the respective rates of the primary end point ings of the primary analysis (Table S9 in the were 8. In addition, to account for the the results of multivariate analyses showed a protocol change in October 2006 whereby the similar protective effect of the two Mediterra intensity of dietary intervention in the control nean diets versus the control diet with respect to group was increased, we compared hazard ratios n engl j med 368;14 nejm. Kaplan–Meier Estimates of the Incidence of Outcome Events in the Total Study Population. Panel A shows the incidence of the primary end point (a composite of acute myocardial infarction, stroke, and death from cardiovascular causes), and Panel B shows total mortality. Hazard ratios were stratified according to center (Cox model with robust variance estimators. Shown are adjusted hazard ratios for the primary end point within specific subgroups. Squares denote hazard ratios; horizontal lines represent 95% confidence intervals. Hazard ratios indicate the relative risk in both intervention groups merged together (vs. Scores for adherence to the Mediterranean diet range from 0 to 14, with higher scores indicating greater adherence. They are particularly relevant given the reduction of approximately 30%, among high challenges of achieving and maintaining weight risk persons who were initially free of cardiovas loss. These results support the benefits Study also showed a large reduction in rates of of the Mediterranean diet for cardiovascular risk coronary heart disease events with a modified n engl j med 368;14 nejm. That result, protocol for the control group was changed half however, was based on only a few major events. The lower intensity of There were small between-group differences dietary intervention for the control group during in some baseline characteristics in our trial, which the first few years might have caused a bias to were not clinically meaningful but were statisti ward a benefit in the two Mediterranean-diet cally significant, and we therefore adjusted for groups, since the participants in these two groups these variables. In fully adjusted analyses, we found received a more intensive intervention during significant results for the combined cardiovas that time. However, we found no significant in cular end point and for stroke, but not for myo teraction between the period of trial enrollment cardial infarction alone. Sec but also to a lower statistical power to identify ond, we had losses to follow-up, predominantly effects on myocardial infarction. Our findings in the control group, but the participants who are consistent with those of prior observational dropped out had a worse cardiovascular risk pro studies of the cardiovascular protective effects file at baseline than those who remained in the of the Mediterranean diet,2,5 olive oil,21-23 and study, suggesting a bias toward a benefit in the nuts24,25; smaller trials assessing effects on tra control group. Third, the generalizability of our ditional cardiovascular risk factors6-9 and novel findings is limited because all the study partici risk factors, such as markers of oxidation, in pants lived in a Mediterranean country and were flammation, and endothelial dysfunction6,8,26-28; at high cardiovascular risk; whether the results and studies of conditions associated with high can be generalized to persons at lower risk or to cardiovascular risk — namely, the metabolic other settings requires further research. The pated, with reduced statistical power to sepa results of our trial might explain, in part, the rately assess components of the primary end lower cardiovascular mortality in Mediterranean point. However, favorable trends were seen for countries than in northern European countries both stroke and myocardial infarction. This is take, changes in total fat were small and the consistent with epidemiologic studies that showed largest differences at the end of the trial were in an inverse association between the Mediterra the distribution of fat subtypes. The interventions nean diet2,34 or olive-oil consumption22 and in were intended to improve the overall dietary pat cident stroke. Thus, extra the Womens Health Initiative Dietary Modifica virgin olive oil and nuts were probably respon tion Trial, wherein a low-fat dietary approach sible for most of the observed benefits of the resulted in no cardiovascular benefit. Differences were also ob components of the Mediterranean diet report served for fish and legumes but not for other edly associated with better survival include mod food groups. The small between-group differ erate consumption of ethanol (mostly from wine), ences in the diets during the trial are probably low consumption of meat and meat products, due to the facts that for most trial participants and high consumption of vegetables, fruits, nuts, the baseline diet was similar to the trial Mediter legumes, fish, and olive oil. The results support receiving lecture fees and payment for the development of edu the benefits of the Mediterranean diet for the cational presentations, as well as grant support through his in stitution, from Ferrer; receiving payment for the development of primary prevention of cardiovascular disease. Martínez-González and through Centro de and receiving grant support through his institution from Eroski Investigación Biomédica en Red de Fisiopatología de la Obesi and Nestlé. Mediterranean diet pyramid: a cul herence to the Mediterranean diet on Scientific evidence of interventions using tural model for healthy eating. Am J Clin health: an updated systematic review and the Mediterranean diet: a systematic re Nutr 1995;61:Suppl:1402S-1406S. The role of tree nuts and peanuts in tiative Randomized Controlled Dietary dieticians increased the adherence to the prevention of coronary heart disease: Modification Trial. Food synergy: an operational concept for elderly Mediterranean population of Spain. Salas-Salvadó J, Fernández-Ballart J, cell activation: a molecular antiinflam Copyright © 2013 Massachusetts Medical Society. Abstract Background Recurrent Clostridium difficile infection is difficult to treat, and failure rates for anti From the Departments of Internal Medi biotic therapy are high. The primary end of Gastroenterology, Hagaziekenhuis, the point was the resolution of diarrhea associated with C. Keller at the Aca demic Medical Center, Department of the study was stopped after an interim analysis. Of 16 patients in the infusion Gastroenterology, Meibergdreef 9, 1105 group, 13 (81%) had resolution of C. The 3 remaining patients received a second infusion with feces from a differ keller@hagaziekenhuis. Conclusions the infusion of donor feces was significantly more effective for the treatment of recurrent C. Generally, repeated and extended otic therapy (≥10 days of vancomycin at a dose of courses of vancomycin are prescribed. In this study, donor feces at baseline; admission to an intensive care unit; or were infused in patients with recurrent C. Patients in whom antibi dard vancomycin regimen, and a standard van otic therapy failed were offered treatment with comycin regimen with bowel lavage. Patients who had Infusion of Donor Feces been admitted to referring hospitals were visited Donors (<60 years of age) were volunteers who by the study physicians, who performed the ran were initially screened using a questionnaire ad domization. All participants provided written in dressing risk factors for potentially transmissible formed consent. Donor feces were screened for parasites board monitored the trial on an ongoing basis. Treponema pallidum; Strongyloides stercoralis; and Ent 408 n engl j med 368;5 nejm. A donor pool was created, and bacterial communities before and after donor screening was repeated every 4 months. Before feces infusion using Simpsons Reciprocal Index of donation, another questionnaire was used to diversity,22 on a scale ranging from 1 to 250, with screen for recent illnesses. Feces were collected by the donor on the day of infusion and immediately transported to the Statistical Analysis hospital. Feces were diluted with 500 ml of ster the objective was to determine the superiority of ile saline (0.

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For infants born vaginally to mothers with a frst-episode genital infection depression test embarrassing bodies cheap zyban 150mg on-line, some experts recommend empiric parenteral acyclovir treatment depression psychology purchase 150mg zyban otc. The sensitivity of viral cultures for detecting neonatal infection in infants whose mothers were treated with antiviral medication near the end of pregnancy is not known mood disorder lamp discount zyban 150mg free shipping. Often anxiety xanax not working generic zyban 150 mg without prescription, primary infections are asymptomatic, in which case the frst symptomatic episode will represent a reactivated recurrent infection. Care of Newborn Infants Whose Mothers Have a History of Genital Herpes But No Active Genital Lesions at Delivery. The risk of transmission to infants by health care professionals who have herpes labialis or who are asymptomatic oral shedders of virus is low. Compromising patient care by excluding health care professionals with cold sores who are essential for the operation of the hospital nursery must be weighed against the potential risk of newborn infants becoming infected. Health care professionals with cold sores who have contact with infants should cover and not touch their lesions and should comply with hand hygiene policies. Health care professionals with an active her petic whitlow should not have responsibility for direct care of neonates or immunocom promised patients and should wear gloves and use hand hygiene during direct care of other patients. Household members with herpetic skin lesions (eg, herpes labialis or herpetic whitlow) should be counseled about the risk and should avoid contact of their lesions with newborn infants by taking the same measures as recommended for infected health care professionals as well as avoid ing kissing and nuzzling the infant while they have active lip lesions or touching the infant while they have herpetic whitlow. These patients should not be kissed by people with cold sores or touched by people with herpetic whitlow. Most of these infections are asymptomatic, with shedding of virus in saliva occurring in the absence of clinical disease. Exclusion of chil dren with cold sores (ie, recurrent infection) from child care or school is not indicated. Children with uncovered lesions on exposed surfaces pose a small potential risk to contacts. Additional control measures include avoiding the sharing of respiratory secretions through contact with objects and washing and sanitizing mouthed toys, bottle nipples, and utensils that have come in contact with saliva. Consideration of suppressive antiviral therapy should be limited to athletes with a history of recurrent herpes gladiatorum or herpes labialis to reduce the risk of reactivation dur ing wrestling season. Clinical manifestations are classifed according to site (pulmonary or disseminated), duration (acute, subacute, or chronic), and pattern (primary or reactiva tion) of infection. Most symptomatic patients have acute pulmonary histoplasmosis, a self limited illness characterized by fever, chills, nonproductive cough, and malaise. Typical radiographic fndings include diffuse interstitial or reticulonodular pulmonary infltrates and hilar or mediastinal adenopathy. Chronic cavitary pulmonary histoplasmosis occurs most often in older adults and can mimic pulmonary tuberculosis. Mediastinal involvement, usually a complication of pulmonary histoplasmosis, includes mediastinal lymphadenitis, which can cause airway encroachment in young children. Infammatory syndromes (pericarditis and rheumatologic syndromes) also can develop; erythema nodosum can occur in adolescents and adults. H capsulatum var duboisii is the cause of African histoplasmosis and is found only in central and western Africa. Infection is acquired through inhalation of conidia from soil, often contaminated with bat guano or bird droppings. The inoculum size, strain virulence, and immune status of the host affect severity of illness. Infections occur sporadically, in outbreaks when weather condi tions (dry and windy) predispose to spread of spores or as point-source epidemics after exposure to activities that disturb contaminated soil. Prior infection confers partial immunity; reinfection can occur but requires a larger inoculum. H capsulatum organ isms from bone marrow, blood, sputum, and tissue specimens grow on standard mycologic media in 1 to 6 weeks. Demonstration of typical intracellular yeast forms by examination with Gomori methenamine silver or other stains of tissue, blood, bone marrow, or bronchoalveolar lavage specimens strongly supports the diagnosis of histoplasmosis when clinical, epide miologic, and other laboratory studies are compatible. Detection of H capsulatum antigen in serum, urine, a bronchoalveolar lavage speci men, or cerebrospinal fuid using a quantitative enzyme immunoassay is possible using a rapid, commercially available diagnostic test. Antigen detection in blood and urine specimens is most sensitive for severe, acute pulmonary infections and for progressive disseminated infections. Results often transiently are positive early in the course of acute, self-limited pulmonary infections. If the result initially is positive, the antigen test also is useful for monitoring treatment response and, after treatment, identifying relapse. Cross-reactions occur in patients with blastomy cosis, coccidioidomycosis, paracoccidioidomycosis, and penicilliosis; clinical and epide miologic circumstances aid in differentiating these infections. Serologic testing also is available and is most useful in patients with subacute or chronic pulmonary disease. A fourfold increase in either yeast-phase or mycelial-phase titers or a single titer of ≥1:32 in either test is presumptive evidence of active or recent infection. Cross-reacting antibodies can result from Blastomyces dermatitidis and Coccidioides species infections. The immunodiffusion test is more specifc than the complement fxa tion test, but the complement fxation test is more sensitive. Itraconazole 1 is preferred over other azoles by most experts; when used in adults, itraconazole is more effective, has fewer adverse effects, and is less likely to induce resistance than fuconazole. Although safety and effcacy of itraconazole for use in children have not been established, anecdotal experience has found it to be well tolerated and effective. Serum concentrations of itraconazole should be determined to ensure that effective, nontoxic levels are attained. Immunocompetent children with uncomplicated acute pulmonary histoplasmosis rarely require antifungal therapy, because infection usually is self-limited. If the patient is symptomatic for more than 4 weeks, itraconazole should be given for 6 to 12 weeks, although the effectiveness of this treatment is not well documented. For severe acute pulmonary infections, treatment with amphotericin B is recommended for 1 to 2 weeks. After clinical improvement occurs, itraconazole is recommended for an additional 12 weeks. Methylprednisolone during the frst 1 to 2 weeks of therapy can be used if respira tory complications develop. Clinical practice guidelines for the management of patients with histoplasmosis: 2007 update by the Infectious Diseases Society of America. Severe cases initially should be treated with amphotericin B followed by itraconazole for the same duration. Mediastinal and infammatory manifestations of infection generally do not need to be treated with antifungal agents. However, mediastinal adenitis that causes obstruction of a bronchus, the esophagus, or another mediastinal structure may improve with a brief course of corticosteroids. In these instances, itraconazole should be used concurrently and continued for 6 to 12 weeks. Dense fbrosis of mediastinal structures without an associated granulomatous infammatory component does not respond to antifungal therapy, and surgical intervention may be necessary. Pericarditis and rheumatologic syndromes may respond to treatment with nonsteroidal anti-infammatory agents (indomethacin. For treatment of progressive disseminated histoplasmosis in a nonimmunocompro mised infant or child, amphotericin B is the drug of choice and is given for 4 to 6 weeks. An alternative regimen uses induction with amphotericin B therapy for 2 to 4 weeks and, when there has been substantial clinical improvement and a decline in the serum concen tration of histoplasmosis antigen, oral itraconazole is administered for 12 weeks. Longer periods of therapy can be required for patients with severe disease, primary immunode fciency syndromes, acquired immunodefciency that cannot be reversed, or patients who experience relapse despite appropriate therapy. Stable, low concentra tions of urine antigen that are not accompanied by signs of active infection may not nec essarily require prolongation or resumption of treatment. Exposure to soil and dust from areas with signifcant accumulations of bird and bat droppings should be avoided, especially by immunocompromised people. If exposure is unavoidable, it should be minimized through use of appropriate respiratory protec tion (eg, N95 respirator), gloves, and disposable clothing. Old structures likely to have been contaminated with bird or bat droppings should be moistened thoroughly before demolition. Guidelines for preventing histoplasmosis have been designed for health and safety professionals, environmental consultants, and people supervising workers involved in activities in which contaminated materials are disturbed.

As one anatomy professor put it to me neurotic depression definition cheap zyban 150mg with mastercard, You wouldnt tell a patient the gory details of a surgery if that would make them not consent mood disorder code buy generic zyban line. It was the thought of your mother mood disorder vs personality disorder buy zyban 150 mg low cost, your father anxiety 10 year old boy purchase zyban 150 mg mastercard, your grandparents being hacked to pieces by wisecracking twenty-two-year-old medical students. Every time I read the pre-lab and saw a term like bone saw, I wondered if this would be the session in which I finally vomited. Yet I was rarely troubled in lab, even when I found that the bone saw in question was nothing more than a common, rusty wood saw. The closest I ever came to vomiting was nowhere near the lab but on a visit to my grandmothers grave in New York, on the twentieth anniversary of her death. I found myself doubled over, almost crying, and apologizing—not to my cadaver but to my cadavers grandchildren. In the midst of our lab, in fact, a son requested his mothers half-dissected body back. But by the time youd skinned the limbs, sliced through inconvenient muscles, pulled out the lungs, cut open the heart, and removed a lobe of the liver, it was hard to recognize this pile of tissue as human. Anatomy lab, in the end, becomes less a violation of the sacred and more something that interferes with happy hour, and that realization discomfits. Seeing the body as matter and mechanism is the flip side to easing the most profound human suffering. By the same token, the most profound human suffering becomes a mere pedagogical tool. Anatomy professors are perhaps the extreme end of this relationship, yet their kinship to the cadavers remains. Early on, when I made a long, quick cut through my donors diaphragm in order to ease finding the splenic artery, our proctor was both livid and horrified. Not because I had destroyed an important structure or misunderstood a key concept or ruined a future dissection but because I had seemed so cavalier about it. The look on his face, his inability to vocalize his sadness, taught me more about medicine than any lecture I would ever attend. When I explained that another anatomy professor had told me to make the cut, our proctors sadness turned to rage, and suddenly red-faced professors were being dragged into the hallway. Once, while showing us the ruins of our donors pancreatic cancer, the professor asked, How old is this fellow? As medical students, we were confronted by death, suffering, and the work entailed in patient care, while being simultaneously shielded from the real brunt of responsibility, though we could spot its specter. Med students spend the first two years in classrooms, socializing, studying, and reading; it was easy to treat the work as a mere extension of undergraduate studies. But my girlfriend, Lucy, whom I met in the first year of medical school (and who would later become my wife), understood the subtext of the academics. The squiggly lines on that page were more than just lines; they were ventricular fibrillation deteriorating to asystole, and they could bring you to tears. Lucy and I attended the Yale School of Medicine when Shep Nuland still lectured there, but I knew him only in my capacity as a reader. Nuland was a renowned surgeon-philosopher whose seminal book about mortality, How We Die, had come out when I was in high school but made it into my hands only in medical school. Few books I had read so directly and wholly addressed that fundamental fact of existence: all organisms, whether goldfish or grandchild, die. I pored over it in my room at night, and remember in particular his description of his grandmothers illness, and how that one passage so perfectly illuminated the ways in which the personal, medical, and spiritual all intermingled. Nuland recalled how, as a child, he would play a game in which, using his finger, he indented his grandmothers skin to see how long it took to resume its shape—a part of the aging process that, along with her ikindlebooks. By the time Bubbeh stopped praying, she had stopped virtually everything else as well. Descriptions like Nulands convinced me that such things could be known only face-to-face. I was pursuing medicine to bear witness to the twinned mysteries of death, its experiential and biological manifestations: at once deeply personal and utterly impersonal. In an act of desperation, he cut open the patients chest and tried to pump his heart manually, tried to literally squeeze the life back into him. The patient died, and Nuland was found by his supervisor, covered in blood and failure. Medical school had changed by the time I got there, to the point where such a scene was simply unthinkable: as medical students, we were barely allowed to touch patients, let alone open their chests. What had not changed, though, was the heroic spirit of responsibility amid blood and failure. I had recently taken Step 1 of my medical boards, wrapping up two years of intensive study buried in books, deep in libraries, poring over lecture notes in coffee shops, reviewing hand-made flash cards while lying in bed. The next two years, then, I would spend in the hospital and clinic, finally putting that theoretical knowledge to use to relieve concrete suffering, with patients, not abstractions, as my primary focus. Walking into the building as the sun descended, I tried to recall the stages of labor, the corresponding dilation of the cervix, the names of the stations that indicated the babys descent—anything that might prove helpful when the time came. As a medical student, my task was to learn by observation and avoid getting in the way. Residents, who had finished medical school and were now completing training in a chosen specialty, and nurses, with their years of clinical experience, would serve as my primary instructors. But the fear still lurked—I could feel its fluttering —that through accident or expectation, Id be called on to deliver a child by myself, and fail. The mother lay in a bed, resting, quiet, monitor bands wrapped around her belly, tracking her contractions and the twins heart rates and sending the signal to the screens Id seen at the nurses station. The father stood at the bedside holding his wifes hand, worry etched on his brow. I tried decoding the indecipherable scribbles in Garcias chart, which was like reading hieroglyphics, and came away with the knowledge that her first name was Elena, this was her second pregnancy, she had received no prenatal care, and she had no insurance. I wrote down the names of the drugs she was getting and made a note to look them up later. I read a little about premature labor in a textbook I found in the doctors lounge. Preemies, if they survived, apparently incurred high rates of brain hemorrhages and cerebral palsy. I walked over to the nurse and asked her to teach me how to read those little squiggles on the monitor, which were no clearer to me than the doctors handwriting but could apparently foretell calm or disaster. She nodded and began talking me through reading a contraction and the fetal hearts reaction to it, the way, if you looked closely, you could see— She stopped. Without a word, she got up and ran into Elenas room, then burst back out, grabbed the phone, and paged Melissa. A minute later, Melissa arrived, bleary-eyed, glanced at the strips, and rushed into the patients room, with me trailing behind. She flipped open her cellphone and called the attending, rapidly talking in a jargon I only partially understood. The twins were in distress, I gathered, and their only shot at survival was an emergency C-section. A nurse frantically painted the womans swollen abdomen with an antiseptic solution, while the attending, the resident, and I splashed alcohol cleanser on our hands and forearms. I mimicked their urgent strokes, standing silently as they cursed under their breath. The anesthesiologists intubated the patient while the senior surgeon, the attending, fidgeted. I tried to follow every movement, digging in my brain for textbook anatomical sketches. He sliced confidently through the tough white rectus fascia covering the muscle, then split the fascia and ikindlebooks. He sliced that open as well, and a small face appeared, then disappeared amid the blood. In plunged the doctors hands, pulling out one, then two purple babies, barely moving, eyes fused shut, like tiny birds fallen too soon from a nest. With their bones visible through translucent skin, they looked more like the preparatory sketches of children than children themselves. With the immediate danger averted, the pace of the operation slowed, frenzy turning to something resembling calm. The uterus was sutured back together, the stitches like a row of teeth, biting closed the open wound. To me, the wound looked like a mass of disorganized tissue, yet to the surgeons it had an appreciable order, like a block of marble to a sculptor.