PubMed Health⌕ Search

Biomedical subjects

I Gerling

Publications and source records attributed to I Gerling.

At least 19 recordsLinked to original sources
PubMed2003

Forensic pathological aspects of postmortem imaging of gunshot injury to the head: documentation and biometric data.

To determine the value of imaging procedures such as computer tomography (CT) and magnetic resonance imaging (MRI) of the head in providing additional information of forensic relevance, we examined 17 cadavers of human victims of gunshot wounds to the head. Three of the victims briefly survived the gunshot wound. The weapons involved were all guns with low muzzle energy (<550 J), i.e., handguns and low-velocity rifles. In the majority of cases ( n=15) a penetrating wound to the head was found, only two cases showed the bullet lodged in the brain. In some cases, imaging of the skull and brain was performed prior to autopsy; in others imaging took place after autopsy on the isolated, formalin-fixed brain. The imaging findings were correlated with the criminological data and the results of macroscopic and microscopic examination of the brain. The findings on the bony structures of the head provided imaging criteria for differentiation between entrance and exit of the gunshot wounds, which corresponded to the forensic pathological findings at autopsy. CT scans and MRI of the cerebral parenchyma revealed lanes of opaque bone and missile fragments along the course of the missile, which allowed recognition of the missile track in 3D reconstruction. Biometric reconstruction allowed easy determination of the angle of the missile track in all three planes. Examination of the parenchymal structures and imaging of the isolated, formalin-fixed brain enabled tracking of the missile path directly along the zone of destruction as well as demonstration of secondary changes such as air bubbles along the bullet course, hemorrhage and edema. The significance of a translucent zone surrounding the missile track in several cases remains unclear; it probably represents tissue destruction secondary to temporary cavitation. The imaging procedures described here allowed excellent documentation of in situ conditions, while the storing of data enabled biometric reconstruction for determination of the angle of trajectory, of entrance and exit wounds, and the extent of tissue damage along the missile track and, possibly, in the zone of temporary cavitation.

Adult↗
PubMed2001

Death from thermal effects and burns.

One hundred and fifteen unselected autopsy cases of death from thermal effects and/or fire between 1990 and 1999 were analyzed with regard to time of death, signs of vitality at the scene of the fire, the manner and cause of death, and the extent of soft tissue loss. The cases represented approximately 6% of all autopsy cases at the Institute of Legal Medicine responsible for a catchment area with approximately 700,000 inhabitants. In 23 victims suffering burn injuries, death occurred during initial medical care or clinical treatment. The causes of death were primary respiratory arrest due to smoke poisoning or delayed shock caused by thermal injuries to the skin. Death occurred at the scene of the fatal event in 85 cases: eight cases exhibited no thermal effects; the cause of death in one of these cases was polytrauma incurred in a leap from a height; in seven cases there was poisoning due to smoke inhalation. The remaining 77 cases were characterized by signs of intensive thermal and/or fire effects. Clear signs of vitality (carboxyhemoglobin (COHb) in blood, inhalation and/or swallowing of soot) were found in 84.7% of the victims dying at the site of the fatal event. Of the 13 victims showing no signs of vitality at the scene, a cause of death could be determined in only seven cases; death in the other six cases remains unexplained. Quantification of the soft tissue loss revealed a possible correlation with the temperature and time course of heat exposure.

Adolescent↗
PubMed2001

Creutzfeldt-Jakob disease (CJD) in a case of suspected chronic heavy metal poisoning.

We describe a patient who died of suspected heavy metal poisoning after a nine-month history of rapidly worsening dementia. Autopsy at a forensic-pathological institute established the postmortem diagnosis of sporadic Creutzfeldt-Jakob disease (CJD) based on demonstration of the proteinase-resistant prion protein (PrPsSc) in Western-Blot on native brain tissue. Microscopic examination of the macroscopically largely inconspicuous brain revealed marked spongiform changes in the gray matter--mainly affecting the cerebral cortex, nucleus caudatus, and putamen--with confluent vacuoles. Patchy or perivacuolar deposits of PrPSc were found as well as granular PrPsc deposits. The cerebellum contained focal PrPsc deposits. There was an astrogliosis in the white matter and a proliferation of microglia in the gray matter with a simultaneous clear reduction in neuronal elements. The differential diagnosis is discussed, as is the potential risk to those performing autopsy on forensic cases with a clinical picture of rapidly progressing dementia, especially in cases where a prion disease is not initially suspected.

Brain↗
PubMed2000

Petechiae of the baby's skin as differentiation symptom of infanticide versus SIDS.

The successive killing of three siblings by their biological mother at two-year intervals is described. The children were 367 days, 75 days and 3 years old. Although sudden infant death syndrome (SIDS) or interstitial pneumonia could not be ruled out as the cause of death in the two younger children, who were killed first, the third child exhibited discrete signs of violence in the mouth and throat area which were interpreted as proof of infanticide. All three children had petechiae of the skin of the face and throat, the upper thorax, the shoulders and the mucous membranes of the mouth. None of the children exhibited signs of a disease-related hemorrhagic tendency. After the mother was convicted of murdering the three-year-old boy by smothering in combination with compression of the thorax, she confessed to having killed the other two children in a similar manner. In the absence of hemostatic disease, the presence of petechiae of the skin extending over the entire drainage area of the Vena cava superior can be regarded as evidence of an increase in pressure in the thoracic cavity secondary to obstruction of the airways with simultaneous chest compression.

Asphyxia↗
PubMed2000

Sudden unexpected infant death due to fibroma of the heart.

A 7-month-old previously healthy female infant was found dead in her crib by her mother shortly after having been laid down to sleep following the noontime feeding. Because the child did not suffer from an acute illness and no other evidence pointed to a cause of death, it was initially assumed by the police that she had died of sudden infant death syndrome. At autopsy, however, the cause of death was determined to be cardiac arrhythmia secondary to fibroma of the heart.

Cause of Death↗
PubMed1997

Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent.

MHC class II alleles clearly contribute a primary genetic component of susceptibility to autoimmune insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice. However, IDDM does not occur in NOD mice made MHC class I-deficient by a functionally inactivated beta2-microglobulin allele (beta2m(null)). In the present study the beta2m(null) mutation was used to examine the relative contributions of MHC class I and class II-dependent T cell responses for initiating autoimmune pancreatic beta cell destruction in NOD mice. Splenocytes from diabetic NOD donors transferred IDDM to both lymphocyte-deficient NOD-scid (class I+) and NOD-scid.beta2m(null) mice (class I-). In contrast, splenocytes from young prediabetic NOD donors only transferred IDDM to class I+, but not class I- NOD-scid recipients. However, splenocytes from prediabetic NOD donors did transfer IDDM to NOD-scid.beta2m(null) recipients previously engrafted with class I+, but not class I-, pancreatic islets. CD4+ T cell lines reactive against some syngeneic class I+ targets could be isolated from NOD.beta2m(null) mice. However, NOD.beta2m(null) T cells underwent activation-driven deletion when transferred into class I+ NOD-scid recipients. Hence, the class I autoreactive T cells present in NOD.beta2m(null) donors did not elicit IDDM when transferred into class I+ NOD-scid recipients. Collectively, these results show that autoimmune IDDM in NOD mice is initiated by MHC class I-dependent T cell responses, but this leads to the subsequent activation of additional T cell populations that can mediate pancreatic beta cell destruction in a MHC class I-independent manner.

Adoptive Transfer↗
PubMed1993

Myocardial fibrosis--a rare complication in patients with cystic fibrosis.

We report a 10-month-old male infant who was admitted to our hospital with a history of failure to thrive and bulky stools. On examination, he was dystrophic and had a protruding abdomen, but he was well oxygenated and his lungs were clear on auscultation. A tachycardia of 145 beats per min and radiological evidence of cardiomegaly indicated involvement of the heart, but an ECG failed to show signs of myocarditis or cardiac hypertrophy. An elevated sweat chloride concentration of 141 mEq/l confirmed the diagnosis of cystic fibrosis (CF). Molecular analysis revealed heterozygosity for the common mutation delta F508. He died unexpectedly of a sudden cardiac arrest 2 days later. Autopsy revealed scattered myocardial necrosis and fibrosis. Some 50 documented cases of myocardial fibrosis in infants with CF have been reported. Suggested causes such as malnourishment and hypovitaminosis remain speculative as systematic studies have yet to be done.

Cardiomegaly↗
PubMed1993

Lack of 64,000-M(r) islet autoantigen overexpression and antibody development following coxsackievirus B4 infection in diabetes-resistant mice.

Congenic B10.BR/SgSnJ H-2kTlaa mice were infected with a diabetogenic strain of coxsackievirus CB4 to correlate abnormalities of sugar metabolism with virus replication in islets, 64,000-M(r) (64K) islet autoantigen expression, 64K antibody development, and pancreas histopathology in early and late infection. Plaque assay was used to measure virus replication, whereas immunoprecipitation of the mouse islet extracts with 64K antibody-positive and -negative human sera measured autoantigen expression and antibody development. The infected mice exhibited blood glucose values below that of the noninfected control animals at 72 h postinfection, this subnormal blood glucose persisted at 6 wk postinfection and later. A baseline expression of the autoantigen was detected in the noninfected mice; however, the infected animals did not overexpress the protein at 72 h postinfection or develop 64K antibodies after infection. Limited virus replication was detected in the islets at 72 h postinfection but not later. Acinar necrosis, but not islet loss due to mononuclear cell infiltration, was evident in the infected mice. The congenic mice did not develop hyperglycemia and appear to be diabetes-resistant, their beta cells were largely preserved. This may be due to limited virus replication in their islets or their failure to overexpress the autoantigen and develop 64K antibodies following the infection. Diabetes-susceptible mice, on the contrary, support active virus replication in their islets, overexpress the autoantigen at 72 h postinfection, and develop 64K antibodies and hyperglycemia following such infection (Gerling et al., 1988, 1991).

Animals↗
PubMed1991

Coxsackievirus B4-induced development of antibodies to 64,000-Mr islet autoantigen and hyperglycemia in mice.

Diabetogenic Coxsackievirus B4 infection produces a diabetes syndrome in susceptible mice resembling insulin-dependent diabetes mellitus. We reported a two- to threefold increased expression of a 64,000-Mr (64 K) islet autoantigen in the infected mice preceding the development of hyperglycemia, suggesting a possible role of the virus in autoimmunity. To assess if the virus could be a trigger of autoimmunity, 64 K autoantibody development was correlated with hyperglycemia and virus replication in islets during early and late infection. Additionally, the effects of blood removal from these mice on the incidence of hyperglycemia and antibody production were evaluated. Noninfected control mice were essentially 64 K antibody negative, the infected consistently positive. Approximately 30% of the animals developed antibodies by 72 h postinfection (p.i.) and 90% by 4-6 wk p.i. Virus-induced hyperglycemia appeared bimodal: hyperglycemia in 50% of the mice by 1 wk p.i., which decreased to 30% by 3 wk and then increased to 80-100% by 6 wk p.i. Infectious virus was abundant in the islets at 72 h but undetectable later. Hyperglycemia seen at 6 wk decreased dramatically (67-73%) if the mice were bled once between 72 h and 2 wk p.i. Only 50-60% of the mice bled once were 64 K positive compared to 90% positive nonbled mice. Coxsackievirus may initiate or enhance the autoimmune response.

Animals↗
PubMed1990

[Use of rectal temperature-time of death nomograms at the scene of death].

The application of the rectal temperature time of death nomogram at the scene of death by 11 authors from 6 lego-medical institutes resulted in a standard deviation of the differences between nomographic and real death time of +/- 1.3 h in 46 cases (group I) with met requirements and clearly defined points of contact, nevertheless, including 9 cases with a more progressive cooling (0.5 greater than Q greater than or equal to 0.2). In cases with a real death time of more than 4h (N = 26) the standard deviation was +/- 1.0 hours corresponding to permissible variation of 95% of +/- 2.0 hours. Consequently, the permissible variation of 95% was much smaller than that suggested by the nomogram. The nomographic death time interval did not agree with the real one in 5 cases out of additional 30 cases with recognizably unsure points of contact (group II).

Body Temperature Regulation↗
PubMed1989

Pancreatic D-cell disorder in coxsackievirus B4-induced diabetic mice.

Pancreatic D-cell disorder was analyzed in Coxsackievirus B4-induced diabetic mice employing molecular hybridization with a radiolabelled probe to quantitate somatostatin mRNA, and specific immunoprecipitation to measure somatostatin synthesis and its release. Many infected mice showed blood glucose lower than noninfected control animals at 72 h postinfection and 85% became hyperglycemic at 6-8 weeks postinfection. Pancreatic somatostatin decreased by 24% and 43% at 72 h and 6 weeks postinfection, respectively, while somatostatin release in islets from the infected mice increased by 2-fold or more. Residual islet somatostatin content after release was initially higher than control at 72 h and then declined at 6 weeks. Islet cellular RNA content decreased by 35% at 6 weeks, somatostatin mRNA content decreased by approximately 45% at 72 h and 6 weeks postinfection. D-cell disorder - somatostatin mRNA supply, synthesis, and release - is clearly evident in this model, which could be of significance in type I diabetes.

Animals↗
PubMed1988

Purification and characterization of a strain of coxsackievirus B4 of human origin that induces diabetes in mice.

A diabetogenic strain of coxsackievirus B4 of human origin has been purified to study its biochemistry and diabetogenicity. Tissue culture cells infected with the virus contain two distinct types of particles--virions and membrane-bound virions (MBV). MBVs are lighter (p = 1.29) than virions (p = 1.34), and they contain relatively more protein than RNA. Virons contain four capsid proteins, VPI-4, of various molecular weights: VP1, 37,500; VP2, 36,000; VP3, 26,000; and VP4, 5,500. MBVs contain three of these proteins and several additional proteins of molecular weights 45,000 to greater than 92,500, possibly of host or viral origin. The RNA in each type of particle is a 35S molecule; T1 oligonucleotide fingerprint profiles suggest minor differences in the two RNAs. Hybridization experiments show a great deal of sequence homology between the RNA of the diabetogenic strain and the RNA of prototype CB4, which does not induce overt diabetes. MBVs are 10-70 times less infective than virions, yet they are more pathogenic in mice and induce significantly higher glucose intolerance (hyperglycemia). The hyperglycemic response appears to be lower in mice infected with both types of particles than in mice infected with MBVs alone. Thus, the two subpopulations of virions present in the diabetogenic strain differ biochemically and in their ability to induce diabetes.

Animals↗
PubMed1988

Effect of coxsackievirus B4 infection in mice on expression of 64,000-Mr autoantigen and glucose sensitivity of islets before development of hyperglycemia.

Diabetogenic strains of Coxsackievirus B4 (CB4) produce a diabetes syndrome in susceptible mice that resembles insulin-dependent diabetes mellitus. To assess the possible role of autoimmunity, the expression of a 64,000-Mr islet antigen in SJL/J and CD1 mice infected with a diabetogenic strain of CB4 was monitored in early and late infection. Additionally, virus-induced abnormalities in glucose metabolism were correlated with several changes in purified islets to assess beta-cell physiology. Over 80% of the mice exhibited subnormal blood glucose at 72 h postinfection (p.i.) and were hyperglycemic at 6 and 8 wk p.i. Islet yield in infected mice decreased by 29-47% at 72 h and 6 wk p.i. compared to noninfected mice. Insulin release stimulated by 16.7 mM glucose increased greater than twofold at 72 h p.i. but declined at 6 wk well below the level of noninfected mice. Likewise, residual islet insulin content after release also increased at 72 h and then declined. Total protein synthesis in the islets decreased by 30% at 72 h and by 60% at 6 wk p.i. Although the synthesis of five proteins of heterogeneous molecular weights, including tubulin, was severely depressed in the infected islets at 72 h p.i. compared with control islets or islets at 6 wk p.i., synthesis of the 64,000-Mr component and another protein of 36,000 Mr increased by two- to threefold. It is possible that CB4 infection may initiate or enhance an autoimmune reaction by increased expression of the 64,000-Mr antigen.

Animals↗
PubMed1986

Islet cell and 64K autoantibodies are associated with plasma IgG in newly diagnosed insulin-dependent diabetic children.

There is a high prevalence of islet cell antibodies (ICA) and autoantibodies detected against an islet cell protein of Mr 64,000 at the time of clinical diagnosis of insulin-dependent diabetes (IDDM). In view of the biphasic immune response after antigen presentation, the purpose of this study was to determine the presence of ICA and antibodies against the 64,000 islet antigen after separation of IgM from IgG to prevent interference between the two antibody classes. Plasma samples from 10 newly diagnosed IDDM children and 10 healthy controls were precipitated with polyethylene glycol (PEG), and the crude Ig was subjected to Sephacryl S-300 chromatography to separate IgM and IgG. ICA determined by indirect immunofluorescence on frozen sections of human pancreas showed reduced background immunofluorescence intensity in the purified fractions compared with crude plasma. The number of ICA-positive samples among the IDDM patients increased from 7/10 in plasma to 9/10 in the IgG fraction. There was an increase in the ICA titer in 6/9 of the positive samples. All purified IgM samples were ICA negative. Immunoprecipitation experiments by using Nonidet P-40 detergent lysates of [35S]methionine-labeled neonatal rat islets demonstrated that the 64,000 autoantibodies were in the IgG fraction. We found 7/10 IDDM samples to be positive, whereas all controls were negative. The background in the autoradiographic analysis was markedly reduced in the IgG fractions compared with immunoprecipitates with crude or PEG-purified plasma and the IgM fraction. ICA titers did not correlate to the ability of the IgG fraction to precipitate the 64,000 autoantigen. It is concluded that both the ICA and 64,000 autoantibodies are primarily of the IgG class at the time of clinical onset of IDDM, and that purification of IgG from human IDDM plasma facilitates the detection of the rat islet cell 64,000 antigen.

Animals↗
PubMed1985

Immunological aspects of type 1 and 2 diabetes mellitus.

IDDM occurs predominantly among individuals being class II antigen HLA-DR 3 and/or 4 positive, while NIDDM is not associated with HLA-D. Although the HLA-DR 3 or 4 specificities are prerequisites for IDDM to develop, their high frequencies (about 60%) in the background population preclude tissue typing as a predictive test, underlined by the observation that less than 50% of monozygotic twins are concordant for IDDM. The presence of a number of immune abnormalities argues that the causes of IDDM may be sought in an altered immune reaction against antigens present in the pancreatic B cells and/or in the environment. The majority of IDDM patients of short duration show both cellular and humoral autoimmunity against the pancreatic B cells. Similar phenomena may be observed in patients initially diagnosed as NIDDM and treated with oral hypoglycemic agents. It has been speculated that these patients have a retarded form of IDDM. It is possible that the combination of specific Class II antigen molecule(s) and an invading antigen (virus, bacterium, chemical etc.) presented to the immune system triggers the formation of effector cells such as B lymphocytes and cytotoxic T lymphocytes which also cross-react with the pancreatic B cells. Multiple exposures to this or related antigens throughout several years may eventually lead a sufficient loss of pancreatic B cells to cause insulin dependence.

Antibody Formation↗