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Given that Peter Rossi himself has said he no longer believes it, it safe to say it’s probably not true:[1]“The laws as stated give the false impression that they rest on empirical data. However, I did not undertake anything that might be remotely called empirical research. I had certainly read a rather large number of evaluations reports and articles. I had formed a strong impression at the time that most evaluations done in the decades before 1982 had found programs ineffective. I still do not have or know of any empirical studies of the outcomes of all program evaluations or any reasonable sample of program evaluations, although there are a fairly large number of meta-analyses that summarize outcomes of evaluations dealing with some specific substantive areas. Based on my continued reading of evaluations, impressions are now different…It should be quite obvious that currently I believe that the Iron and Stainless Steel Laws cannot be taken seriously as originally stated. “Footnotes[1] http://welfareacademy.org/rossi/Rossi_Remarks_Iron_Law_Reconsidered.pdf

to this day, the program had taken a steep descend from whatever it was intended to mean. i would like to make a list of cons here,lab and research Facilities: firstly there is no a separate department for the course. they r to share the classrooms with mech students. That becomes worse during the labs, we dont have facilities required. That being said, students spend most of their time polishing the same old samples repeatedly or in xeroxing the observation and record notebooks. SEM is shown as an exhibition visit.Faculty: Literally the faculty -student ratio is at its worst. people of a class even after forming groups of 3, cannot get a guide induvidualy for each group. its impossible to find a friendly staff. The faculty behave as if we are long term enemies without any reason. if u r to be marked as a non confirming part, u r sure to be awarded an U or even a series of Us in that teachers subjects. everybody in the department, even the lab assistants, HOD office people all treat u the worst. u could expect “why should i sign this” or “u look like a gay to me” from the hod office, if you want a sign in a scholarship or some sort of application.It is just another school where u r not forced to study. the syllabus is 8 yrs old. i guess the students look as obnoxious retards in the eyes of professors, that u become a shit for them.and there is a new trend, the faculty form a union kind of a thing among themselves, so that they can give a fail to a student in the other subjects. There are lots of untold miseries students at materials science dept face.I would just like to tell to those persons who thinks they can help the students, PLEASE SHUT DOWN THE DEPARTMENT so that no other student is to suffer. if there could be a referendum about this seen to that identity is made anonymous, i believe every student in the department would echo the same.I mentioned about anonymity in particular because only in this college they force u give a feedback or evaluation form with name so that it would be easy for them to target. this really happened during the feedback session for Metal forming class, that was just at the end of lab model exam.

While I was in training in the midwest, I had an autopsy with a somewhat unusual clinical history, which I received on only three sheets of paper, one from the EMTs who had been called to his home, one from the intake triage nurse at the emergency department of the hospital, and the third from the emergency department physician who talked with the patient’s wife briefly.The patient was a male in his late 20s with a history of chronic alcoholism. He was found by the EMTs to be unresponsive, and his blood glucose level when they initially evaluated him with a POC (point of care) test was zero. They hung some D5/NS (5% glucose in normal saline) and brought him to the hospital. He was an insulin-dependent diabetic who had been drinking very heavily for several days, and the three histories were discordant on one point: the first said he had been taking his insulin, the second said he hadn’t, and the third said he hadn’t, but his wife knew that he needed it, so she gave it to him, but didn’t know how to measure it up. That explained the glucose reading. The patient was mildly febrile, decidedly tachycardic, and quite obtunded. I can’t remember what the other laboratory results were. He was transferred to the ICU and died as he arrived there.At autopsy, performed at 10 hours post-mortem, the patient was seen to be a well-nourished, normally-developed male who appeared his stated age. The first thing one does after checking the paperwork (is there a properly executed autopsy permit?), identifying the body (toe tag, wristband, or whatever), and performing an external examination is to draw some blood samples, which I did. I then began the dissection. Behind me, I heard a small “pop!” I turned around. The blood sample tube had blown its top! At this point, I already had a diagnosis. The patient had a massive infection with gas-forming bacteria, and because of the speed of this development, probably an anaerobic species. The gross appearance of the organs of the body showed two particular abnormalities:The lining of the arterial vessels and the left side of the heart showed normal pink-tan coloration. The right side of the heart and the lining of large veins showed a purple-gray color. (One will encounter “pink-tan” twenty times in the course of the usual gross autopsy description, and “purple-gray” almost never, except for the description of the capsule of the spleen.)The distal stomach and the duodenum were soft and grayish-brown, indicating early decay, a highly unusual finding in a patient who undergoes a prompt post-mortem examination.On the basis of the behavior of the blood sample (pop!), the gross findings described above, and the blood bacterial culture (positive for Clostridium perfringens) and Gram stain results on the gastric and duodenal microscopic sections (Gram-positive spore-forming rods), we had a case of small bowel clostridial enteritis. The difference in the arterial and venous circulation was due to the higher oxygen content of the arterial blood, which kept the anaerobic bacteria from proliferating in that part of the circulation, whereas in the lower-oxygen environment of the venous side, the bacteria grew, and, releasing proteolytic enzymes, caused breakdown of the red cells with staining of the endothelial linings.This disease is virtually never seen in the U.S. (I think one case in a diabetic woman who did survive made it onto a medical mystery TV program). It was noted in post-war (WWII) Scandinavia and Germany, where it was called “Darmbrand” (“burning guts” in German) and is presently confined to Papua-New Guinea, where it is called “Pig-bel,” pidgin English for “pig belly,” because of its onset in natives who eat pig rarely, in a ceremony where the whole, un-eviscerated pig is thrown into a pit filled with hot coals and then eaten by everyone in the village after the cooking is finished. Predisposing factors are protein-poor nutrition (which results in a lower level of proteolytic digestive enzymes in the stomach) and exposure to clostridial spores.In the case of the Papuans, this cooking of the pig with included intestines will spread the clostridial spores from the pig’s gut (where they form only a small minority of the intestinal flora) onto the rest of the meat, and as the Papuans are usually on a rather protein-poor diet, they’ll also have a lower lever of protein-digesting enzymes, which is thought to render them more susceptible to infection by the Clostridia.In post-war Europe, protein deficiency was widespread. If there was any increase in environmental Clostridia, I’m unaware of it.In the case of our patient, his stomach contained some partially digested lima beans. Although he had good body habitus, he was somewhat malnourished from his binge drinking of a few days, and the beans may have contributed legume trypsin inhibitor (which interferes with protein digestion) to the mix, as well as the immunosuppression that occurs in diabetes mellitus. How much the severe hypoglycemia contributed to the patient’s course I cannot say.Finally, it is said that resting pulse rate in the presence of fever increases at about 10 bpm (beats per minute) with each degree of temperature rise. In clostridial infection, the increase is much higher, explaining the tachycardia. (This finding is non-specific, as many things can cause tachycardia.)